Pub Date : 2024-10-18DOI: 10.1186/s12943-024-02158-w
Joshua E Allen, Gabriel Krigsfeld, Luv Patel, Patrick A Mayes, David T Dicker, Gen Sheng Wu, Wafik S El-Deiry
<p><b>Correction</b><b>: </b><b>Mol Cancer 14, 99 (2015)</b></p><p><b>https://doi.org/10.1186/s12943-015-0346-9</b></p><br/><p>Following publication of the original article [1], the authors reported inadvertent errors in two panels of Figure 3.</p><p>The original Figure 3B shows a duplication of a histological image. The duplicated image has been replaced and the images, as well as their labels, have been accurately arranged in the corrected Figure 3. In addition, the attached corrected Figure 3 revises two time point labels in panel E.</p><p>The following clarification was added to figure legend 3E: “A portion of the control and ONC201/TIC10 results shown for reference were previously published [26].” The corrected and incorrect figures are given below.</p><p>Incorrect Figure 3:</p><figure><picture><source srcset="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02158-w/MediaObjects/12943_2024_2158_Figa_HTML.png?as=webp" type="image/webp"/><img alt="figure a" aria-describedby="Figa" height="743" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02158-w/MediaObjects/12943_2024_2158_Figa_HTML.png" width="685"/></picture></figure><p>Correct Figure 3:</p><figure><picture><source srcset="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02158-w/MediaObjects/12943_2024_2158_Figb_HTML.png?as=webp" type="image/webp"/><img alt="figure b" aria-describedby="Figb" height="603" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02158-w/MediaObjects/12943_2024_2158_Figb_HTML.png" width="685"/></picture></figure><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Allen JE, Krigsfeld G, Patel L, et al. Identification of TRAIL-inducing compounds highlights small molecule ONC201/TIC10 as a unique anti-cancer agent that activates the TRAIL pathway. Mol Cancer. 2015;14:99. https://doi.org/10.1186/s12943-015-0346-9.</p><p>Article PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use xlink:href="#icon-eds-i-download-medium" xmlns:xlink="http://www.w3.org/1999/xlink"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>Departments of Medicine, Genetics, and Pharmacology, Laboratory of Molecular Oncology and Cell Cycle Regulation, University of Pennsylvania School of Medicine, Philadelphia, 19104, PA, USA</p><p>Joshua E Allen, Gabriel Krigsfeld, Luv Patel, Patrick A Mayes, David T Dicker & Wafik S El-Deiry</p></li><li><p>Current affiliation: Oncoceutics, Inc., Hummelstown, PA, USA</p><p>Joshua E Allen</p></li><li><p>Department of Medical Oncology and Molecular Therapeutics Program, Laboratory of Translational Oncology and Experimental Cancer Therapeutics, Fox Chase Cancer Center, Philadelphia, 19111, PA, USA</p><p>David T Dicker & Wa
更正：Mol Cancer 14, 99 (2015)https://doi.org/10.1186/s12943-015-0346-9Following，原文章[1]发表后，作者报告了图3两个面板中的无心之失。原图3B显示了一张重复的组织学图像。在更正后的图 3 中，重复的图像已被替换，图像及其标签也已准确排列。此外，附图 3 更正了面板 E 中的两个时间点标签。在图例 3E 中添加了以下说明："对照组和 ONC201/TIC10 的部分结果供参考，这些结果之前已发表[26]"。更正和错误的图如下。错误的图 3：正确的图 3：Allen JE, Krigsfeld G, Patel L, et al. TRAIL 诱导化合物的鉴定突出了小分子 ONC201/TIC10 作为激活 TRAIL 通路的独特抗癌剂的作用。Mol Cancer.2015;14:99. https://doi.org/10.1186/s12943-015-0346-9.Article PubMed PubMed Central Google Scholar Download references作者和所属单位医学、遗传学和药理学系，分子肿瘤学和细胞周期调节实验室，宾夕法尼亚大学医学院，费城，19104，宾夕法尼亚州，美国Joshua E Allen, Gabriel Krigsfeld, Luv Patel, Patrick A Mayes, David T Dicker & Wafik S El-DeiryCurrent affiliation：Oncoceutics, Inc、Hummelstown, PA, USAJoshua E AllenDepartment of Medical Oncology and Molecular Therapeutics Program, Laboratory of Translational Oncology and Experimental Cancer Therapeutics, Fox Chase Cancer Center, Philadelphia, 19111, PA, USDavid T Dicker &；Wafik S El-DeiryDepartment of Pathology, Program in Molecular Biology and Genetics, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI, 48201、USAGen Sheng WuAuthorsJoshua E AllenView author publications您也可以在PubMed Google ScholarGabriel KrigsfeldView author publications您也可以在PubMed Google ScholarLuv PatelView author publications您也可以在PubMed Google ScholarLuv PatelView author publications您也可以在PubMed Google ScholarPatrick A Mayes查看作者发表的文章ScholarPatrick A MayesView 作者发表作品您也可以在 PubMed Google ScholarDavid T DickerView 作者发表作品您也可以在 PubMed Google ScholarGen Sheng WuView 作者发表作品您也可以在 PubMed Google ScholarWafik S El-Deiry查看作者发表的文章您也可以在PubMed Google Scholar中搜索该作者通讯作者Wafik S El-Deiry.开放存取 本文采用知识共享署名-非商业性-禁止衍生 4.0 国际许可协议进行许可，该协议允许以任何媒介或格式进行任何非商业性使用、共享、分发和复制，只要您适当注明原作者和来源，提供知识共享许可协议的链接，并说明您是否修改了许可材料。根据本许可协议，您无权分享源自本文或本文部分内容的改编材料。本文中的图片或其他第三方材料均包含在文章的知识共享许可协议中，除非在材料的信用栏中另有说明。如果材料未包含在文章的知识共享许可协议中，且您打算使用的材料不符合法律规定或超出了许可使用范围，则您需要直接获得版权所有者的许可。要查看该许可的副本，请访问 http://creativecommons.org/licenses/by-nc-nd/4.0/.Reprints and permissionsCite this articleAllen, J.E., Krigsfeld, G., Patel, L. et al. Correction：TRAIL诱导化合物的鉴定凸显了小分子 ONC201/TIC10 作为激活 TRAIL 通路的独特抗癌剂的作用。Mol Cancer 23, 233 (2024). https://doi.org/10.1186/s12943-024-02158-wDownload citationPublished: 18 October 2024DOI: https://doi.org/10.1186/s12943-024-02158-wShare this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative
{"title":"Correction: Identification of TRAIL-inducing compounds highlights small molecule ONC201/TIC10 as a unique anti-cancer agent that activates the TRAIL pathway","authors":"Joshua E Allen, Gabriel Krigsfeld, Luv Patel, Patrick A Mayes, David T Dicker, Gen Sheng Wu, Wafik S El-Deiry","doi":"10.1186/s12943-024-02158-w","DOIUrl":"https://doi.org/10.1186/s12943-024-02158-w","url":null,"abstract":"<p><b>Correction</b><b>: </b><b>Mol Cancer 14, 99 (2015)</b></p><p><b>https://doi.org/10.1186/s12943-015-0346-9</b></p><br/><p>Following publication of the original article [1], the authors reported inadvertent errors in two panels of Figure 3.</p><p>The original Figure 3B shows a duplication of a histological image. The duplicated image has been replaced and the images, as well as their labels, have been accurately arranged in the corrected Figure 3. In addition, the attached corrected Figure 3 revises two time point labels in panel E.</p><p>The following clarification was added to figure legend 3E: “A portion of the control and ONC201/TIC10 results shown for reference were previously published [26].” The corrected and incorrect figures are given below.</p><p>Incorrect Figure 3:</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02158-w/MediaObjects/12943_2024_2158_Figa_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure a\" aria-describedby=\"Figa\" height=\"743\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02158-w/MediaObjects/12943_2024_2158_Figa_HTML.png\" width=\"685\"/></picture></figure><p>Correct Figure 3:</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02158-w/MediaObjects/12943_2024_2158_Figb_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure b\" aria-describedby=\"Figb\" height=\"603\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02158-w/MediaObjects/12943_2024_2158_Figb_HTML.png\" width=\"685\"/></picture></figure><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Allen JE, Krigsfeld G, Patel L, et al. Identification of TRAIL-inducing compounds highlights small molecule ONC201/TIC10 as a unique anti-cancer agent that activates the TRAIL pathway. Mol Cancer. 2015;14:99. https://doi.org/10.1186/s12943-015-0346-9.</p><p>Article PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>Departments of Medicine, Genetics, and Pharmacology, Laboratory of Molecular Oncology and Cell Cycle Regulation, University of Pennsylvania School of Medicine, Philadelphia, 19104, PA, USA</p><p>Joshua E Allen, Gabriel Krigsfeld, Luv Patel, Patrick A Mayes, David T Dicker & Wafik S El-Deiry</p></li><li><p>Current affiliation: Oncoceutics, Inc., Hummelstown, PA, USA</p><p>Joshua E Allen</p></li><li><p>Department of Medical Oncology and Molecular Therapeutics Program, Laboratory of Translational Oncology and Experimental Cancer Therapeutics, Fox Chase Cancer Center, Philadelphia, 19111, PA, USA</p><p>David T Dicker & Wa","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"7 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142448577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-17DOI: 10.1186/s12943-024-02152-2
Léa Montégut, Peng Liu, Liwei Zhao, María Pérez-Lanzón, Hui Chen, Misha Mao, Shuai Zhang, Lisa Derosa, Julie Le Naour, Flavia Lambertucci, Silvia Mingoia, Uxía Nogueira-Recalde, Rafael Mena-Osuna, Irene Herranz-Montoya, Nabil Djouder, Sylvain Baulande, Hui Pan, Adrien Joseph, Meriem Messaoudene, Bertrand Routy, Marine Fidelle, Tarek Ben Ahmed, Olivier Caron, Pierre Busson, David Boulate, Mélanie Deschasaux-Tanguy, Nathalie Arnault, Jonathan G. Pol, Eliane Piaggio, Mathilde Touvier, Laurence Zitvogel, Suzette Delaloge, Isabelle Martins, Guido Kroemer
<p><b>Correction: Mol Cancer 23 187 (2024)</b></p><p><b>https://doi.org/10.1186/s12943-024-02098-5</b></p><p>Following publication of the original article [1], the authors noticed a minor but significant error in the representation of the author name Tarek Ben Ahmed as “Ben” was captured as given name instead of a family name. Thus, in the online version, the name Tarek Ben Ahmed was mistakenly listed as Ahmed TB instead of Ben Ahmed T. The original article has been corrected.</p><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Montégut L, Liu P, Zhao L. et al. Acyl-coenzyme a binding protein (ACBP) - a risk factor for cancer diagnosis and an inhibitor of immunosurveillance. Mol Cancer. 2024;23:187. https://doi.org/10.1186/s12943-024-02098-5</p></li></ol><p>Download references<svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use xlink:href="#icon-eds-i-download-medium" xmlns:xlink="http://www.w3.org/1999/xlink"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>Centre de Recherche des Cordeliers, Université Paris Cité, Sorbonne Université, Equipe labellisée par la Ligue Contre le Cancer, Inserm U1138, Paris, France</p><p>Léa Montégut, Peng Liu, Liwei Zhao, María Pérez-Lanzón, Hui Chen, Misha Mao, Shuai Zhang, Julie Le Naour, Flavia Lambertucci, Silvia Mingoia, Uxía Nogueira-Recalde, Hui Pan, Adrien Joseph, Jonathan G. Pol, Isabelle Martins & Guido Kroemer</p></li><li><p>Metabolomics and Cell Biology Platforms, Gustave Roussy Institut, Villejuif, France</p><p>Léa Montégut, Peng Liu, Liwei Zhao, María Pérez-Lanzón, Hui Chen, Misha Mao, Shuai Zhang, Julie Le Naour, Flavia Lambertucci, Uxía Nogueira-Recalde, Hui Pan, Jonathan G. Pol, Laurence Zitvogel, Isabelle Martins & Guido Kroemer</p></li><li><p>Faculté de Médecine, Université de Paris Saclay, Kremlin Bicêtre, Paris, France</p><p>Léa Montégut, Hui Chen, Lisa Derosa, Julie Le Naour, Hui Pan & Laurence Zitvogel</p></li><li><p>Department of Respiratory and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China</p><p>Shuai Zhang</p></li><li><p>Equipe Labellisée Par la Ligue Contre le Cancer, Inserm U1015, Gustave Roussy, Villejuif, France</p><p>Lisa Derosa, Marine Fidelle, Laurence Zitvogel & Suzette Delaloge</p></li><li><p>Department of Pharmacological Sciences, University of Piemonte Orientale, Novara, Italia</p><p>Silvia Mingoia</p></li><li><p>Grupo de Investigación en Reumatología (GIR), Instituto de Investigación Biomédica de A Coruña (INIBIC), Fundación Profesor Novoa Santos, A Coruña, Spain</p><p>Uxía Nogueira-Recalde</p></li><li><p>Department of Translational Research, Institute Curie Research Center, INSERM U932, PSL Research University, Paris, France</p><p>Rafael Mena-Osuna & Eliane Piaggio</p></li><li><p>Growth Factors, Nutrients and Cancer Group, Molecular Oncology Programme, Centro Nacional de Inv
更正：Mol Cancer 23 187 (2024)https://doi.org/10.1186/s12943-024-02098-5Following 原文[1]发表后，作者注意到在表述作者姓名Tarek Ben Ahmed时出现了一个微小但重要的错误，因为 "Ben "被当作姓氏而不是名字。因此，在网络版中，塔里克-本-艾哈迈德（Tarek Ben Ahmed）被误列为艾哈迈德-塔布（Ahmed TB），而不是本-艾哈迈德-塔布（Ben Ahmed T）。Mol Cancer.2024;23:187. https://doi.org/10.1186/s12943-024-02098-5下载参考文献作者及单位巴黎市立大学索邦大学Cordeliers研究中心，巴黎抗癌联盟Equipe labellisée par la Ligue Contre le Cancer，Inserm U1138，巴黎、FranceLéa Montégut、Peng Liu、Liwei Zhao、María Pérez-Lanzón、Hui Chen、Misha Mao、Shuai Zhang、Julie Le Naour、Flavia Lambertucci、Silvia Mingoia、Uxía Nogueira-Recalde、Hui Pan、Adrien Joseph、Jonathan G．Pol, Isabelle Martins & Guido KroemerMetabolomics and Cell Biology Platforms, Gustave Roussy Institut, Villejuif, FranceLéa Montégut, Peng Liu, Liwei Zhao, María Pérez-Lanzón, Hui Chen, Misha Mao, Shuai Zhang, Julie Le Naour, Flavia Lambertucci, Uxía Nogueira-Recalde, Hui Pan, Jonathan G., J., J., J., J., J., J., J., J.
{"title":"Correction: Acyl-coenzyme a binding protein (ACBP) - a risk factor for cancer diagnosis and an inhibitor of immunosurveillance","authors":"Léa Montégut, Peng Liu, Liwei Zhao, María Pérez-Lanzón, Hui Chen, Misha Mao, Shuai Zhang, Lisa Derosa, Julie Le Naour, Flavia Lambertucci, Silvia Mingoia, Uxía Nogueira-Recalde, Rafael Mena-Osuna, Irene Herranz-Montoya, Nabil Djouder, Sylvain Baulande, Hui Pan, Adrien Joseph, Meriem Messaoudene, Bertrand Routy, Marine Fidelle, Tarek Ben Ahmed, Olivier Caron, Pierre Busson, David Boulate, Mélanie Deschasaux-Tanguy, Nathalie Arnault, Jonathan G. Pol, Eliane Piaggio, Mathilde Touvier, Laurence Zitvogel, Suzette Delaloge, Isabelle Martins, Guido Kroemer","doi":"10.1186/s12943-024-02152-2","DOIUrl":"https://doi.org/10.1186/s12943-024-02152-2","url":null,"abstract":"<p><b>Correction: Mol Cancer 23 187 (2024)</b></p><p><b>https://doi.org/10.1186/s12943-024-02098-5</b></p><p>Following publication of the original article [1], the authors noticed a minor but significant error in the representation of the author name Tarek Ben Ahmed as “Ben” was captured as given name instead of a family name. Thus, in the online version, the name Tarek Ben Ahmed was mistakenly listed as Ahmed TB instead of Ben Ahmed T. The original article has been corrected.</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Montégut L, Liu P, Zhao L. et al. Acyl-coenzyme a binding protein (ACBP) - a risk factor for cancer diagnosis and an inhibitor of immunosurveillance. Mol Cancer. 2024;23:187. https://doi.org/10.1186/s12943-024-02098-5</p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>Centre de Recherche des Cordeliers, Université Paris Cité, Sorbonne Université, Equipe labellisée par la Ligue Contre le Cancer, Inserm U1138, Paris, France</p><p>Léa Montégut, Peng Liu, Liwei Zhao, María Pérez-Lanzón, Hui Chen, Misha Mao, Shuai Zhang, Julie Le Naour, Flavia Lambertucci, Silvia Mingoia, Uxía Nogueira-Recalde, Hui Pan, Adrien Joseph, Jonathan G. Pol, Isabelle Martins & Guido Kroemer</p></li><li><p>Metabolomics and Cell Biology Platforms, Gustave Roussy Institut, Villejuif, France</p><p>Léa Montégut, Peng Liu, Liwei Zhao, María Pérez-Lanzón, Hui Chen, Misha Mao, Shuai Zhang, Julie Le Naour, Flavia Lambertucci, Uxía Nogueira-Recalde, Hui Pan, Jonathan G. Pol, Laurence Zitvogel, Isabelle Martins & Guido Kroemer</p></li><li><p>Faculté de Médecine, Université de Paris Saclay, Kremlin Bicêtre, Paris, France</p><p>Léa Montégut, Hui Chen, Lisa Derosa, Julie Le Naour, Hui Pan & Laurence Zitvogel</p></li><li><p>Department of Respiratory and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China</p><p>Shuai Zhang</p></li><li><p>Equipe Labellisée Par la Ligue Contre le Cancer, Inserm U1015, Gustave Roussy, Villejuif, France</p><p>Lisa Derosa, Marine Fidelle, Laurence Zitvogel & Suzette Delaloge</p></li><li><p>Department of Pharmacological Sciences, University of Piemonte Orientale, Novara, Italia</p><p>Silvia Mingoia</p></li><li><p>Grupo de Investigación en Reumatología (GIR), Instituto de Investigación Biomédica de A Coruña (INIBIC), Fundación Profesor Novoa Santos, A Coruña, Spain</p><p>Uxía Nogueira-Recalde</p></li><li><p>Department of Translational Research, Institute Curie Research Center, INSERM U932, PSL Research University, Paris, France</p><p>Rafael Mena-Osuna & Eliane Piaggio</p></li><li><p>Growth Factors, Nutrients and Cancer Group, Molecular Oncology Programme, Centro Nacional de Inv","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"11 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142443910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-16DOI: 10.1186/s12943-024-02150-4
Jae-Hyeok Kang, Nizam Uddin, Seungmo Kim, Yi Zhao, Ki-Chun Yoo, Min-Jung Kim, Sung-Ah Hong, Sangsu Bae, Jeong-Yeon Lee, Incheol Shin, Young Woo Jin, Heather M. O’Hagan, Joo Mi Yi, Su-Jae Lee
Triple-negative breast cancer (TNBC), the most aggressive subtype, presents a critical challenge due to the absence of approved targeted therapies. Hence, there is an urgent need to identify effective therapeutic targets for this condition. While epidermal growth factor receptor (EGFR) is prominently expressed in TNBC and recognized as a therapeutic target, anti-EGFR therapies have yet to gain approval for breast cancer treatment due to their associated side effects and limited efficacy. Here, we discovered that intercellular adhesion molecule-1 (ICAM-1) exhibits elevated expression levels in metastatic breast cancer and serves as a pivotal binding adaptor for EGFR activation, playing a crucial role in malignant progression. The activation of EGFR by tumor-expressed ICAM-1 initiates biased signaling within the JAK1/STAT3 pathway, consequently driving epithelial-to-mesenchymal transition and facilitating heightened metastasis without influencing tumor growth. Remarkably, ICAM-1-neutralizing antibody treatment significantly suppressed cancer metastasis in a breast cancer orthotopic xenograft mouse model. In conclusion, our identification of ICAM-1 as a novel tumor intrinsic regulator of EGFR activation offers valuable insights for the development of TNBC-specific anti-EGFR therapies.
{"title":"Tumor-intrinsic role of ICAM-1 in driving metastatic progression of triple-negative breast cancer through direct interaction with EGFR","authors":"Jae-Hyeok Kang, Nizam Uddin, Seungmo Kim, Yi Zhao, Ki-Chun Yoo, Min-Jung Kim, Sung-Ah Hong, Sangsu Bae, Jeong-Yeon Lee, Incheol Shin, Young Woo Jin, Heather M. O’Hagan, Joo Mi Yi, Su-Jae Lee","doi":"10.1186/s12943-024-02150-4","DOIUrl":"https://doi.org/10.1186/s12943-024-02150-4","url":null,"abstract":"Triple-negative breast cancer (TNBC), the most aggressive subtype, presents a critical challenge due to the absence of approved targeted therapies. Hence, there is an urgent need to identify effective therapeutic targets for this condition. While epidermal growth factor receptor (EGFR) is prominently expressed in TNBC and recognized as a therapeutic target, anti-EGFR therapies have yet to gain approval for breast cancer treatment due to their associated side effects and limited efficacy. Here, we discovered that intercellular adhesion molecule-1 (ICAM-1) exhibits elevated expression levels in metastatic breast cancer and serves as a pivotal binding adaptor for EGFR activation, playing a crucial role in malignant progression. The activation of EGFR by tumor-expressed ICAM-1 initiates biased signaling within the JAK1/STAT3 pathway, consequently driving epithelial-to-mesenchymal transition and facilitating heightened metastasis without influencing tumor growth. Remarkably, ICAM-1-neutralizing antibody treatment significantly suppressed cancer metastasis in a breast cancer orthotopic xenograft mouse model. In conclusion, our identification of ICAM-1 as a novel tumor intrinsic regulator of EGFR activation offers valuable insights for the development of TNBC-specific anti-EGFR therapies.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"75 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142440196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-12DOI: 10.1186/s12943-024-02137-1
Lin Chen, Yu-Xin Xu, Yuan-Shuo Wang, Ying-Ying Ren, Xue-Man Dong, Pu Wu, Tian Xie, Qi Zhang, Jian-Liang Zhou
Prostate cancer (PCa) is one of the most prevalent malignancies in males worldwide. Increasing research attention has focused on the PCa microenvironment, which plays a crucial role in tumor progression and therapy resistance. This review aims to provide a comprehensive overview of the key components of the PCa microenvironment, including immune cells, vascular systems, stromal cells, and microbiota, and explore their implications for diagnosis and treatment. Keywords such as “prostate cancer”, “tumor microenvironment”, “immune cells”, “vascular system”, “stromal cells”, and “microbiota” were used for literature retrieval through online databases including PubMed and Web of Science. Studies related to the PCa microenvironment were selected, with a particular focus on those discussing the roles of immune cells, vascular systems, stromal cells, and microbiota in the development, progression, and treatment of PCa. The selection criteria prioritized peer-reviewed articles published in the last five years, aiming to summarize and analyze the latest research advancements and clinical relevance regarding the PCa microenvironment. The PCa microenvironment is highly complex and dynamic, with immune cells contributing to immunosuppressive conditions, stromal cells promoting tumor growth, and microbiota potentially affecting androgen metabolism. Vascular systems support angiogenesis, which fosters tumor expansion. Understanding these components offers insight into the mechanisms driving PCa progression and opens avenues for novel therapeutic strategies targeting the tumor microenvironment. A deeper understanding of the PCa microenvironment is crucial for advancing diagnostic techniques and developing precision therapies. This review highlights the potential of targeting the microenvironment to improve patient outcomes, emphasizing its significance in the broader context of PCa research and treatment innovation.
{"title":"Prostate cancer microenvironment: multidimensional regulation of immune cells, vascular system, stromal cells, and microbiota","authors":"Lin Chen, Yu-Xin Xu, Yuan-Shuo Wang, Ying-Ying Ren, Xue-Man Dong, Pu Wu, Tian Xie, Qi Zhang, Jian-Liang Zhou","doi":"10.1186/s12943-024-02137-1","DOIUrl":"https://doi.org/10.1186/s12943-024-02137-1","url":null,"abstract":"Prostate cancer (PCa) is one of the most prevalent malignancies in males worldwide. Increasing research attention has focused on the PCa microenvironment, which plays a crucial role in tumor progression and therapy resistance. This review aims to provide a comprehensive overview of the key components of the PCa microenvironment, including immune cells, vascular systems, stromal cells, and microbiota, and explore their implications for diagnosis and treatment. Keywords such as “prostate cancer”, “tumor microenvironment”, “immune cells”, “vascular system”, “stromal cells”, and “microbiota” were used for literature retrieval through online databases including PubMed and Web of Science. Studies related to the PCa microenvironment were selected, with a particular focus on those discussing the roles of immune cells, vascular systems, stromal cells, and microbiota in the development, progression, and treatment of PCa. The selection criteria prioritized peer-reviewed articles published in the last five years, aiming to summarize and analyze the latest research advancements and clinical relevance regarding the PCa microenvironment. The PCa microenvironment is highly complex and dynamic, with immune cells contributing to immunosuppressive conditions, stromal cells promoting tumor growth, and microbiota potentially affecting androgen metabolism. Vascular systems support angiogenesis, which fosters tumor expansion. Understanding these components offers insight into the mechanisms driving PCa progression and opens avenues for novel therapeutic strategies targeting the tumor microenvironment. A deeper understanding of the PCa microenvironment is crucial for advancing diagnostic techniques and developing precision therapies. This review highlights the potential of targeting the microenvironment to improve patient outcomes, emphasizing its significance in the broader context of PCa research and treatment innovation. ","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"207 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142415636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-11DOI: 10.1186/s12943-024-02138-0
Ki-Jun Ryu, Ki Won Lee, Seung-Ho Park, Taeyoung Kim, Keun-Seok Hong, Hyemin Kim, Minju Kim, Dong Woo Ok, Gu Neut Bom Kwon, Young-Jun Park, Hyuk-Kwon Kwon, Cheol Hwangbo, Kwang Dong Kim, J Eugene Lee, Jiyun Yoo
Breast cancer remains a significant health concern, with triple-negative breast cancer (TNBC) being an aggressive subtype with poor prognosis. Epithelial-mesenchymal transition (EMT) is important in early-stage tumor to invasive malignancy progression. Snail, a central EMT component, is tightly regulated and may be subjected to proteasomal degradation. We report a novel proteasomal independent pathway involving chaperone-mediated autophagy (CMA) in Snail degradation, mediated via its cytosolic interaction with HSC70 and lysosomal targeting, which prevented its accumulation in luminal-type breast cancer cells. Conversely, Snail predominantly localized to the nucleus, thus evading CMA-mediated degradation in TNBC cells. Starvation-induced CMA activation downregulated Snail in TNBC cells by promoting cytoplasmic translocation. Evasion of CMA-mediated Snail degradation induced EMT, and enhanced metastatic potential of luminal-type breast cancer cells. Our findings elucidate a previously unrecognized role of CMA in Snail regulation, highlight its significance in breast cancer, and provide a potential therapeutic target for clinical interventions.
{"title":"Chaperone-mediated autophagy modulates Snail protein stability: implications for breast cancer metastasis.","authors":"Ki-Jun Ryu, Ki Won Lee, Seung-Ho Park, Taeyoung Kim, Keun-Seok Hong, Hyemin Kim, Minju Kim, Dong Woo Ok, Gu Neut Bom Kwon, Young-Jun Park, Hyuk-Kwon Kwon, Cheol Hwangbo, Kwang Dong Kim, J Eugene Lee, Jiyun Yoo","doi":"10.1186/s12943-024-02138-0","DOIUrl":"10.1186/s12943-024-02138-0","url":null,"abstract":"<p><p>Breast cancer remains a significant health concern, with triple-negative breast cancer (TNBC) being an aggressive subtype with poor prognosis. Epithelial-mesenchymal transition (EMT) is important in early-stage tumor to invasive malignancy progression. Snail, a central EMT component, is tightly regulated and may be subjected to proteasomal degradation. We report a novel proteasomal independent pathway involving chaperone-mediated autophagy (CMA) in Snail degradation, mediated via its cytosolic interaction with HSC70 and lysosomal targeting, which prevented its accumulation in luminal-type breast cancer cells. Conversely, Snail predominantly localized to the nucleus, thus evading CMA-mediated degradation in TNBC cells. Starvation-induced CMA activation downregulated Snail in TNBC cells by promoting cytoplasmic translocation. Evasion of CMA-mediated Snail degradation induced EMT, and enhanced metastatic potential of luminal-type breast cancer cells. Our findings elucidate a previously unrecognized role of CMA in Snail regulation, highlight its significance in breast cancer, and provide a potential therapeutic target for clinical interventions.</p>","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"23 1","pages":"227"},"PeriodicalIF":27.7,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11468019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-11DOI: 10.1186/s12943-024-02146-0
Su Yin Lim, Ines Pires da Silva, Nurudeen A. Adegoke, Serigne N. Lo, Alexander M. Menzies, Matteo S. Carlino, Richard A. Scolyer, Georgina V. Long, Jenny H. Lee, Helen Rizos
Immune checkpoint inhibitors (ICIs) have transformed cancer treatment, providing significant benefit to patients across various tumour types, including melanoma. However, around 40% of melanoma patients do not benefit from ICI treatment, and accurately predicting ICI response remains challenging. We now describe a novel and simple approach that integrates immune-associated transcriptome signatures and tumour volume burden to better predict ICI response in melanoma patients. RNA sequencing was performed on pre-treatment (PRE) tumour specimens derived from 32 patients with advanced melanoma treated with combination PD1 and CTLA4 inhibitors. Of these 32 patients, 11 also had early during treatment (EDT, 5–15 days after treatment start) tumour samples. Tumour volume was assessed at PRE for all 32 patients, and at first computed tomography (CT) imaging for the 11 patients with EDT samples. Analysis of the Hallmark IFNγ gene set revealed no association with ICI response at PRE (AUC ROC curve = 0.6404, p = 0.24, 63% sensitivity, 71% specificity). When IFNg activity was evaluated with tumour volume (ratio of gene set expression to tumour volume) using logistic regression to predict ICI response, we observed high discriminative power in separating ICI responders from non-responders (AUC = 0.7760, p = 0.02, 88% sensitivity, 67% specificity); this approach was reproduced with other immune-associated transcriptomic gene sets. These findings were further replicated in an independent cohort of 23 melanoma patients treated with PD1 inhibitor. Hence, integrating tumour volume with immune-associated transcriptomic signatures improves the prediction of ICI response, and suggest that higher levels of immune activation relative to tumour burden are required for durable ICI response.
{"title":"Size matters: integrating tumour volume and immune activation signatures predicts immunotherapy response","authors":"Su Yin Lim, Ines Pires da Silva, Nurudeen A. Adegoke, Serigne N. Lo, Alexander M. Menzies, Matteo S. Carlino, Richard A. Scolyer, Georgina V. Long, Jenny H. Lee, Helen Rizos","doi":"10.1186/s12943-024-02146-0","DOIUrl":"https://doi.org/10.1186/s12943-024-02146-0","url":null,"abstract":"Immune checkpoint inhibitors (ICIs) have transformed cancer treatment, providing significant benefit to patients across various tumour types, including melanoma. However, around 40% of melanoma patients do not benefit from ICI treatment, and accurately predicting ICI response remains challenging. We now describe a novel and simple approach that integrates immune-associated transcriptome signatures and tumour volume burden to better predict ICI response in melanoma patients. RNA sequencing was performed on pre-treatment (PRE) tumour specimens derived from 32 patients with advanced melanoma treated with combination PD1 and CTLA4 inhibitors. Of these 32 patients, 11 also had early during treatment (EDT, 5–15 days after treatment start) tumour samples. Tumour volume was assessed at PRE for all 32 patients, and at first computed tomography (CT) imaging for the 11 patients with EDT samples. Analysis of the Hallmark IFNγ gene set revealed no association with ICI response at PRE (AUC ROC curve = 0.6404, p = 0.24, 63% sensitivity, 71% specificity). When IFNg activity was evaluated with tumour volume (ratio of gene set expression to tumour volume) using logistic regression to predict ICI response, we observed high discriminative power in separating ICI responders from non-responders (AUC = 0.7760, p = 0.02, 88% sensitivity, 67% specificity); this approach was reproduced with other immune-associated transcriptomic gene sets. These findings were further replicated in an independent cohort of 23 melanoma patients treated with PD1 inhibitor. Hence, integrating tumour volume with immune-associated transcriptomic signatures improves the prediction of ICI response, and suggest that higher levels of immune activation relative to tumour burden are required for durable ICI response.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"59 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142405205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-09DOI: 10.1186/s12943-024-02141-5
Ruohan Yang, Jiuwei Cui
Compared to other types of tumor vaccines, RNA vaccines have emerged as promising alternatives to conventional vaccine therapy due to their high efficiency, rapid development capability, and potential for low-cost manufacturing and safe drug delivery. RNA vaccines mainly include mRNA, circular RNA (circRNA), and Self-amplifying mRNA(SAM). Different RNA vaccine platforms for different tumors have shown encouraging results in animal and human models. This review comprehensively describes the advances and applications of RNA vaccines in antitumor therapy. Future directions for extending this promising vaccine platform to a wide range of therapeutic uses are also discussed.
{"title":"Advances and applications of RNA vaccines in tumor treatment","authors":"Ruohan Yang, Jiuwei Cui","doi":"10.1186/s12943-024-02141-5","DOIUrl":"https://doi.org/10.1186/s12943-024-02141-5","url":null,"abstract":"Compared to other types of tumor vaccines, RNA vaccines have emerged as promising alternatives to conventional vaccine therapy due to their high efficiency, rapid development capability, and potential for low-cost manufacturing and safe drug delivery. RNA vaccines mainly include mRNA, circular RNA (circRNA), and Self-amplifying mRNA(SAM). Different RNA vaccine platforms for different tumors have shown encouraging results in animal and human models. This review comprehensively describes the advances and applications of RNA vaccines in antitumor therapy. Future directions for extending this promising vaccine platform to a wide range of therapeutic uses are also discussed.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"206 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142385474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p><b>Correction:</b> <b><i>Mol Cancer</i></b> <b>23, 213 (2024)</b></p><p><b>https://doi.org/10.1186/s12943-024-02132-6</b></p><p>Following publication of the original article [1], the authors noticed that the Funding information was not indicated in the article. The details of Funding were included in the revised manuscript that was submitted by the author to production system. The Funding information is given below. The original article has been corrected.</p><p><b>Funding</b></p><p>This work was supported by the National Science and Technology Major Project (Nos. 2023ZD0500102), the National Natural Science Foundation of China (Nos. 82270634), and Clinical Young Talent Project, Eagle breeding Team of Meng Chao Tengfei Project (Eastern Hepatobiliary Surgery Hospital).</p><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Shi J, Zhang Z, Yin H, et al. RNA m6A modification in ferroptosis: implications for advancing tumor immunotherapy. Mol Cancer. 2024;23:213. https://doi.org/10.1186/s12943-024-02132-6.</p><p>Article PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use xlink:href="#icon-eds-i-download-medium" xmlns:xlink="http://www.w3.org/1999/xlink"></use></svg></p><span>Author notes</span><ol><li><p>Jun-xiao Shi, Zhi-chao Zhang, Hao-zan Yin, and Xian-jie Piao contributed equally to this work.</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>The Third Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Naval Medical University, Shanghai, 200438, China</p><p>Jun-xiao Shi, Zhi-chao Zhang, Xian-jie Piao, Cheng-hu Liu, Qian-jia Liu, Jia-cheng Zhang, Wen-xuan Zhou, Fu-chen Liu, Yue-fan Wang & Hui Liu</p></li><li><p>The Department of Medical Genetics, Naval Medical University, Shanghai, 200433, China</p><p>Hao-zan Yin & Fu Yang</p></li><li><p>Key Laboratory of Biosafety Defense, Ministry of Education, Shanghai, 200433, China</p><p>Fu Yang</p></li><li><p>Shanghai Key Laboratory of Medical Biodefense, Shanghai, 200433, China</p><p>Fu Yang</p></li></ol><span>Authors</span><ol><li><span>Jun-xiao Shi</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Zhi-chao Zhang</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Hao-zan Yin</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Xian-jie Piao</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Cheng-hu Liu</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Qian-jia Liu</span>View author p
更正：Mol Cancer 23, 213 (2024)https://doi.org/10.1186/s12943-024-02132-6Following 原文[1]发表后，作者注意到文章中未标注资助信息。作者在提交给生产系统的修订稿中包含了详细的资助信息。资助信息如下。本文得到了国家科技重大专项（编号：2023ZD0500102）、国家自然科学基金（编号：82270634）、临床青年人才项目、孟超腾飞计划雏鹰培育团队（东方肝胆外科医院）的支持。Mol Cancer.2024;23:213. https://doi.org/10.1186/s12943-024-02132-6.Article PubMed PubMed Central Google Scholar Download references作者注释施俊孝、张志超、尹浩赞和彪贤杰对本工作有同等贡献。作者和工作单位海军军医大学东方肝胆外科医院肝外三科，上海，200438 史俊晓，张志超，彪宪杰，刘成虎，刘乾嘉，张家成，周文轩，刘福臣，王月凡 &；刘辉海军军医大学医学遗传学系，中国上海，200433 殷浩赞 &；Fu Yang教育部生物安全防御重点实验室，上海，200433Fu Yang上海市医学生物防御重点实验室，上海，200433、ChinaFu Yang作者：施俊孝查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者张志超查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者殷浩赞查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者卞宪杰查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者jie PiaoView 作者发表作品您也可以在 PubMed Google ScholarCheng-hu LiuView 作者发表作品您也可以在 PubMed Google ScholarQian-jia LiuView 作者发表作品您也可以在 PubMed Google ScholarJia-cheng ZhangView作者发表论文您也可以在PubMed Google Scholar中搜索该作者Wen-xuan ZhouView作者发表论文您也可以在PubMed Google Scholar中搜索该作者Fu-chen LiuView作者发表论文您也可以在PubMed Google Scholar中搜索该作者Fu YangView作者发表论文您也可以在PubMed Google Scholar中搜索该作者Yue- fan WangView作者发表论文您也可以在PubMed Google Scholar中搜索该作者Yue- fan WangView作者发表论文fan Wang查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者Hui Liu查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者通信作者Fu Yang、王月凡或刘晖。出版者注释施普林格-自然对出版地图和机构隶属关系中的管辖权主张保持中立。原文的在线版本可在以下网址找到：https://doi.org/10.1186/s12943-024-02132-6.Open Access 本文采用知识共享署名-非商业性-禁止衍生 4.0 国际许可协议进行许可，该协议允许以任何媒介或格式进行任何非商业性使用、共享、分发和复制，只要您适当注明原作者和来源，提供知识共享许可协议的链接，并说明您是否修改了许可材料。根据本许可协议，您无权分享源自本文或本文部分内容的改编材料。本文中的图片或其他第三方材料均包含在文章的知识共享许可协议中，除非在材料的信用栏中另有说明。如果材料未包含在文章的知识共享许可协议中，且您打算使用的材料不符合法律规定或超出了许可使用范围，则您需要直接获得版权所有者的许可。如需查看该许可的副本，请访问 http://creativecommons.org/licenses/by-nc-nd/4.0/.Reprints and permissionsCite this articleShi, Jx., Zhang, Zc., Yin, Hz. et al. Correction：RNA m6A在铁变态反应中的修饰：对推进肿瘤免疫疗法的意义。Mol Cancer 23, 225 (2024). https://doi.org/10.1186/s12943-024-02144-2Download citationPublished: 08 October 2024DOI: https://doi.org/10.1186/s12943-024-02144-2Share this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative
{"title":"Correction: RNA m6A modification in ferroptosis: implications for advancing tumor immunotherapy","authors":"Jun-xiao Shi, Zhi-chao Zhang, Hao-zan Yin, Xian-jie Piao, Cheng-hu Liu, Qian-jia Liu, Jia-cheng Zhang, Wen-xuan Zhou, Fu-chen Liu, Fu Yang, Yue-fan Wang, Hui Liu","doi":"10.1186/s12943-024-02144-2","DOIUrl":"https://doi.org/10.1186/s12943-024-02144-2","url":null,"abstract":"<p><b>Correction:</b> <b><i>Mol Cancer</i></b> <b>23, 213 (2024)</b></p><p><b>https://doi.org/10.1186/s12943-024-02132-6</b></p><p>Following publication of the original article [1], the authors noticed that the Funding information was not indicated in the article. The details of Funding were included in the revised manuscript that was submitted by the author to production system. The Funding information is given below. The original article has been corrected.</p><p><b>Funding</b></p><p>This work was supported by the National Science and Technology Major Project (Nos. 2023ZD0500102), the National Natural Science Foundation of China (Nos. 82270634), and Clinical Young Talent Project, Eagle breeding Team of Meng Chao Tengfei Project (Eastern Hepatobiliary Surgery Hospital).</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Shi J, Zhang Z, Yin H, et al. RNA m6A modification in ferroptosis: implications for advancing tumor immunotherapy. Mol Cancer. 2024;23:213. https://doi.org/10.1186/s12943-024-02132-6.</p><p>Article PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><span>Author notes</span><ol><li><p>Jun-xiao Shi, Zhi-chao Zhang, Hao-zan Yin, and Xian-jie Piao contributed equally to this work.</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>The Third Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Naval Medical University, Shanghai, 200438, China</p><p>Jun-xiao Shi, Zhi-chao Zhang, Xian-jie Piao, Cheng-hu Liu, Qian-jia Liu, Jia-cheng Zhang, Wen-xuan Zhou, Fu-chen Liu, Yue-fan Wang & Hui Liu</p></li><li><p>The Department of Medical Genetics, Naval Medical University, Shanghai, 200433, China</p><p>Hao-zan Yin & Fu Yang</p></li><li><p>Key Laboratory of Biosafety Defense, Ministry of Education, Shanghai, 200433, China</p><p>Fu Yang</p></li><li><p>Shanghai Key Laboratory of Medical Biodefense, Shanghai, 200433, China</p><p>Fu Yang</p></li></ol><span>Authors</span><ol><li><span>Jun-xiao Shi</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Zhi-chao Zhang</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Hao-zan Yin</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Xian-jie Piao</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Cheng-hu Liu</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Qian-jia Liu</span>View author p","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"64 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142384151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-07DOI: 10.1186/s12943-024-02125-5
Annapoorna Venkatachalam, Cristina Correia, Kevin L. Peterson, Xianon Hou, Paula A. Schneider, Annabella R. Strathman, Karen S. Flatten, Chance C. Sine, Emily A. Balczewski, Cordelia D. McGehee, Melissa C. Larson, Laura N. Duffield, X. Wei Meng, Nicole D. Vincelette, Husheng Ding, Ann L. Oberg, Fergus J. Couch, Elizabeth M. Swisher, Hu Li, S. John Weroha, Scott H. Kaufmann
Recent studies indicate that replication checkpoint modulators (RCMs) such as inhibitors of CHK1, ATR, and WEE1 have promising monotherapy activity in solid tumors, including platinum-resistant high grade serous ovarian cancer (HGSOC). However, clinical response rates are generally below 30%. While RCM-induced DNA damage has been extensively examined in preclinical and clinical studies, the link between replication checkpoint interruption and tumor shrinkage remains incompletely understood. Here we utilized HGSOC cell lines and patient-derived xenografts (PDXs) to study events leading from RCM treatment to ovarian cancer cell death. These studies show that RCMs increase CDC25A levels and CDK2 signaling in vitro, leading to dysregulated cell cycle progression and increased replication stress in HGSOC cell lines independent of homologous recombination status. These events lead to sequential activation of JNK and multiple BH3-only proteins, including BCL2L11/BIM, BBC3/PUMA and the BMF, all of which are required to fully initiate RCM-induced apoptosis. Activation of the same signaling pathway occurs in HGSOC PDXs that are resistant to poly(ADP-ribose) polymerase inhibitors but respond to RCMs ex vivo with a decrease in cell number in 3-dimensional culture and in vivo with xenograft shrinkage or a significantly diminished growth rate. These findings identify key cell death-initiating events that link replication checkpoint inhibition to antitumor response in ovarian cancer.
{"title":"Proapoptotic activity of JNK-sensitive BH3-only proteins underpins ovarian cancer response to replication checkpoint inhibitors","authors":"Annapoorna Venkatachalam, Cristina Correia, Kevin L. Peterson, Xianon Hou, Paula A. Schneider, Annabella R. Strathman, Karen S. Flatten, Chance C. Sine, Emily A. Balczewski, Cordelia D. McGehee, Melissa C. Larson, Laura N. Duffield, X. Wei Meng, Nicole D. Vincelette, Husheng Ding, Ann L. Oberg, Fergus J. Couch, Elizabeth M. Swisher, Hu Li, S. John Weroha, Scott H. Kaufmann","doi":"10.1186/s12943-024-02125-5","DOIUrl":"https://doi.org/10.1186/s12943-024-02125-5","url":null,"abstract":"Recent studies indicate that replication checkpoint modulators (RCMs) such as inhibitors of CHK1, ATR, and WEE1 have promising monotherapy activity in solid tumors, including platinum-resistant high grade serous ovarian cancer (HGSOC). However, clinical response rates are generally below 30%. While RCM-induced DNA damage has been extensively examined in preclinical and clinical studies, the link between replication checkpoint interruption and tumor shrinkage remains incompletely understood. Here we utilized HGSOC cell lines and patient-derived xenografts (PDXs) to study events leading from RCM treatment to ovarian cancer cell death. These studies show that RCMs increase CDC25A levels and CDK2 signaling in vitro, leading to dysregulated cell cycle progression and increased replication stress in HGSOC cell lines independent of homologous recombination status. These events lead to sequential activation of JNK and multiple BH3-only proteins, including BCL2L11/BIM, BBC3/PUMA and the BMF, all of which are required to fully initiate RCM-induced apoptosis. Activation of the same signaling pathway occurs in HGSOC PDXs that are resistant to poly(ADP-ribose) polymerase inhibitors but respond to RCMs ex vivo with a decrease in cell number in 3-dimensional culture and in vivo with xenograft shrinkage or a significantly diminished growth rate. These findings identify key cell death-initiating events that link replication checkpoint inhibition to antitumor response in ovarian cancer.\u0000","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"12 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142383732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AlphaFold model has reshaped biological research. However, vast unstructured data in the entire AlphaFold field requires further analysis to fully understand the current research landscape and guide future exploration. Thus, this scientometric analysis aimed to identify critical research clusters, track emerging trends, and highlight underexplored areas in this field by utilizing machine-learning-driven informatics methods. Quantitative statistical analysis reveals that the AlphaFold field is enjoying an astonishing development trend (Annual Growth Rate = 180.13%) and global collaboration (International Co-authorship = 33.33%). Unsupervised clustering algorithm, time series tracking, and global impact assessment point out that Cluster 3 (Artificial Intelligence-Powered Advancements in AlphaFold for Structural Biology) has the greatest influence (Average Citation = 48.36 ± 184.98). Additionally, regression curve and hotspot burst analysis highlight “structure prediction” (s = 12.40, R2 = 0.9480, p = 0.0051), “artificial intelligence” (s = 5.00, R2 = 0.8096, p = 0.0375), “drug discovery” (s = 1.90, R2 = 0.7987, p = 0.0409), and “molecular dynamics” (s = 2.40, R2 = 0.8000, p = 0.0405) as core hotspots driving the research frontier. More importantly, the Walktrap algorithm further reveals that “structure prediction, artificial intelligence, molecular dynamics” (Relevance Percentage[RP] = 100%, Development Percentage[DP] = 25.0%), “sars-cov-2, covid-19, vaccine design” (RP = 97.8%, DP = 37.5%), and “homology modeling, virtual screening, membrane protein” (RP = 89.9%, DP = 26.1%) are closely intertwined with the AlphaFold model but remain underexplored, which implies a broad exploration space. In conclusion, through the machine-learning-driven informatics methods, this scientometric analysis offers an objective and comprehensive overview of global AlphaFold research, identifying critical research clusters and hotspots while prospectively pointing out underexplored critical areas.
{"title":"Artificial intelligence alphafold model for molecular biology and drug discovery: a machine-learning-driven informatics investigation","authors":"Song-Bin Guo, Yuan Meng, Liteng Lin, Zhen-Zhong Zhou, Hai-Long Li, Xiao-Peng Tian, Wei-Juan Huang","doi":"10.1186/s12943-024-02140-6","DOIUrl":"https://doi.org/10.1186/s12943-024-02140-6","url":null,"abstract":"AlphaFold model has reshaped biological research. However, vast unstructured data in the entire AlphaFold field requires further analysis to fully understand the current research landscape and guide future exploration. Thus, this scientometric analysis aimed to identify critical research clusters, track emerging trends, and highlight underexplored areas in this field by utilizing machine-learning-driven informatics methods. Quantitative statistical analysis reveals that the AlphaFold field is enjoying an astonishing development trend (Annual Growth Rate = 180.13%) and global collaboration (International Co-authorship = 33.33%). Unsupervised clustering algorithm, time series tracking, and global impact assessment point out that Cluster 3 (Artificial Intelligence-Powered Advancements in AlphaFold for Structural Biology) has the greatest influence (Average Citation = 48.36 ± 184.98). Additionally, regression curve and hotspot burst analysis highlight “structure prediction” (s = 12.40, R2 = 0.9480, p = 0.0051), “artificial intelligence” (s = 5.00, R2 = 0.8096, p = 0.0375), “drug discovery” (s = 1.90, R2 = 0.7987, p = 0.0409), and “molecular dynamics” (s = 2.40, R2 = 0.8000, p = 0.0405) as core hotspots driving the research frontier. More importantly, the Walktrap algorithm further reveals that “structure prediction, artificial intelligence, molecular dynamics” (Relevance Percentage[RP] = 100%, Development Percentage[DP] = 25.0%), “sars-cov-2, covid-19, vaccine design” (RP = 97.8%, DP = 37.5%), and “homology modeling, virtual screening, membrane protein” (RP = 89.9%, DP = 26.1%) are closely intertwined with the AlphaFold model but remain underexplored, which implies a broad exploration space. In conclusion, through the machine-learning-driven informatics methods, this scientometric analysis offers an objective and comprehensive overview of global AlphaFold research, identifying critical research clusters and hotspots while prospectively pointing out underexplored critical areas.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"1 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142377365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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