Pub Date : 2024-09-18DOI: 10.1186/s12943-024-02119-3
Muhammad Tufail, Can-Hua Jiang, Ning Li
Cancer cells undergo significant metabolic reprogramming to support their rapid growth and survival. This study examines important metabolic pathways like glycolysis, oxidative phosphorylation, glutaminolysis, and lipid metabolism, focusing on how they are regulated and their contributions to the development of tumors. The interplay between oncogenes, tumor suppressors, epigenetic modifications, and the tumor microenvironment in modulating these pathways is examined. Furthermore, we discuss the therapeutic potential of targeting cancer metabolism, presenting inhibitors of glycolysis, glutaminolysis, the TCA cycle, fatty acid oxidation, LDH, and glucose transport, alongside emerging strategies targeting oxidative phosphorylation and lipid synthesis. Despite the promise, challenges such as metabolic plasticity and the need for combination therapies and robust biomarkers persist, underscoring the necessity for continued research in this dynamic field.
{"title":"Altered metabolism in cancer: insights into energy pathways and therapeutic targets","authors":"Muhammad Tufail, Can-Hua Jiang, Ning Li","doi":"10.1186/s12943-024-02119-3","DOIUrl":"https://doi.org/10.1186/s12943-024-02119-3","url":null,"abstract":"Cancer cells undergo significant metabolic reprogramming to support their rapid growth and survival. This study examines important metabolic pathways like glycolysis, oxidative phosphorylation, glutaminolysis, and lipid metabolism, focusing on how they are regulated and their contributions to the development of tumors. The interplay between oncogenes, tumor suppressors, epigenetic modifications, and the tumor microenvironment in modulating these pathways is examined. Furthermore, we discuss the therapeutic potential of targeting cancer metabolism, presenting inhibitors of glycolysis, glutaminolysis, the TCA cycle, fatty acid oxidation, LDH, and glucose transport, alongside emerging strategies targeting oxidative phosphorylation and lipid synthesis. Despite the promise, challenges such as metabolic plasticity and the need for combination therapies and robust biomarkers persist, underscoring the necessity for continued research in this dynamic field. ","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"10 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142236218","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 : 2024-09-16DOI: 10.1186/s12943-024-02103-x
Wei Dai, Jianwei Zhou, Ting Chen
Ovarian cancer (OC) is one of the most prevalent and lethal gynecological malignancies, with high mortality primarily due to its aggressive nature, frequent metastasis, and resistance to standard therapies. Recent research has highlighted the critical role of extracellular vesicles (EVs) in these processes. EVs, secreted by living organisms and carrying versatile and bioactive cargoes, play a vital role in intercellular communication. Functionally, the transfer of cargoes orchestrates multiple processes that actively affect not only the primary tumor but also local and distant pre-metastatic niche. Furthermore, their unique biological properties position EVs as novel therapeutic targets and promising drug delivery systems, with potential profound implications for cancer patients. This review summarizes recent progress in EV biology, delving into the intricate mechanisms by which EVs contribute to OC metastasis and drug resistance. It also explores the latest advances and therapeutic potential of EVs in the clinical context of OC. Despite the progress made, EV research in OC remains in its nascent stages. Consequently, this review presents existing research limitations and suggests avenues for future investigation. Altogether, the review aims to elucidate the critical roles of EVs in OC and spotlight their promising potential in this field.
卵巢癌（OC）是发病率最高、致死率最高的妇科恶性肿瘤之一，死亡率高的主要原因是其侵袭性、频繁转移以及对标准疗法的耐药性。最近的研究强调了细胞外囊泡 (EVs) 在这些过程中的关键作用。细胞外小泡由生物体分泌，携带多种生物活性物质，在细胞间通信中发挥着重要作用。从功能上讲，货物的转移协调了多个过程，不仅积极影响原发肿瘤，还影响局部和远处的转移前生态位。此外，EVs 独特的生物特性使其成为新的治疗靶点和有前途的药物输送系统，对癌症患者具有潜在的深远影响。本综述总结了 EV 生物学的最新进展，深入探讨了 EV 促成肿瘤转移和耐药性的复杂机制。它还探讨了 EVs 在 OC 临床中的最新进展和治疗潜力。尽管取得了进展，但对 OC 中 EV 的研究仍处于起步阶段。因此，本综述介绍了现有研究的局限性，并提出了未来研究的途径。总之，本综述旨在阐明 EVs 在 OC 中的关键作用，并强调其在该领域的巨大潜力。
{"title":"Unraveling the extracellular vesicle network: insights into ovarian cancer metastasis and chemoresistance","authors":"Wei Dai, Jianwei Zhou, Ting Chen","doi":"10.1186/s12943-024-02103-x","DOIUrl":"https://doi.org/10.1186/s12943-024-02103-x","url":null,"abstract":"Ovarian cancer (OC) is one of the most prevalent and lethal gynecological malignancies, with high mortality primarily due to its aggressive nature, frequent metastasis, and resistance to standard therapies. Recent research has highlighted the critical role of extracellular vesicles (EVs) in these processes. EVs, secreted by living organisms and carrying versatile and bioactive cargoes, play a vital role in intercellular communication. Functionally, the transfer of cargoes orchestrates multiple processes that actively affect not only the primary tumor but also local and distant pre-metastatic niche. Furthermore, their unique biological properties position EVs as novel therapeutic targets and promising drug delivery systems, with potential profound implications for cancer patients. This review summarizes recent progress in EV biology, delving into the intricate mechanisms by which EVs contribute to OC metastasis and drug resistance. It also explores the latest advances and therapeutic potential of EVs in the clinical context of OC. Despite the progress made, EV research in OC remains in its nascent stages. Consequently, this review presents existing research limitations and suggests avenues for future investigation. Altogether, the review aims to elucidate the critical roles of EVs in OC and spotlight their promising potential in this field.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"22 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142234460","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}
Metastasis has been one of the primary reasons for the high mortality rates associated with tumours in recent years, rendering the treatment of current malignancies challenging and representing a significant cause of recurrence in patients who have undergone surgical tumour resection. Halting tumour metastasis has become an essential goal for achieving favourable prognoses following cancer treatment. In recent years, increasing clarity in understanding the mechanisms underlying metastasis has been achieved. The concept of premetastatic niches has gained widespread acceptance, which posits that tumour cells establish a unique microenvironment at distant sites prior to their migration, facilitating their settlement and growth at those locations. Neutrophils serve as crucial constituents of the premetastatic niche, actively shaping its microenvironmental characteristics, which include immunosuppression, inflammation, angiogenesis and extracellular matrix remodelling. These characteristics are intimately associated with the successful engraftment and subsequent progression of tumour cells. As our understanding of the role and significance of neutrophils in the premetastatic niche deepens, leveraging the presence of neutrophils within the premetastatic niche has gradually attracted the interest of researchers as a potential therapeutic target. The focal point of this review revolves around elucidating the involvement of neutrophils in the formation and shaping of the premetastatic niche (PMN), alongside the introduction of emerging therapeutic approaches aimed at impeding cancer metastasis.
{"title":"Neutrophils in the premetastatic niche: key functions and therapeutic directions","authors":"Jiachi Jia, Yuhang Wang, Mengjia Li, Fuqi Wang, Yingnan Peng, Junhong Hu, Zhen Li, Zhilei Bian, Shuaixi Yang","doi":"10.1186/s12943-024-02107-7","DOIUrl":"https://doi.org/10.1186/s12943-024-02107-7","url":null,"abstract":"Metastasis has been one of the primary reasons for the high mortality rates associated with tumours in recent years, rendering the treatment of current malignancies challenging and representing a significant cause of recurrence in patients who have undergone surgical tumour resection. Halting tumour metastasis has become an essential goal for achieving favourable prognoses following cancer treatment. In recent years, increasing clarity in understanding the mechanisms underlying metastasis has been achieved. The concept of premetastatic niches has gained widespread acceptance, which posits that tumour cells establish a unique microenvironment at distant sites prior to their migration, facilitating their settlement and growth at those locations. Neutrophils serve as crucial constituents of the premetastatic niche, actively shaping its microenvironmental characteristics, which include immunosuppression, inflammation, angiogenesis and extracellular matrix remodelling. These characteristics are intimately associated with the successful engraftment and subsequent progression of tumour cells. As our understanding of the role and significance of neutrophils in the premetastatic niche deepens, leveraging the presence of neutrophils within the premetastatic niche has gradually attracted the interest of researchers as a potential therapeutic target. The focal point of this review revolves around elucidating the involvement of neutrophils in the formation and shaping of the premetastatic niche (PMN), alongside the introduction of emerging therapeutic approaches aimed at impeding cancer metastasis.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"115 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142231339","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 : 2024-09-14DOI: 10.1186/s12943-024-02121-9
Qiang Liu, Yujing Guan, Shenglong Li
<p><b>Correction: Mol Cancer 23, 183 (2024)</b></p><p><b>https://doi.org/10.1186/s12943-024-02095-8</b></p><p>Following publication of the original article [1], the author reported that the published PDF version is incorrect as the information such as “(See Fig. 5)”, “(Fig. 4; Table 3)”, and “[170]” need to be removed and updated accordingly as shown below. The original article has been corrected.</p><p>The sentences currently read:</p><p> Understanding these regulatory mechanisms and identifying new targets for modifying PD-1/PD-L1 are crucial for advancing precise immunotherapies for genitourinary malignancies (See Fig. 5).</p><p>Therefore, understanding the regulatory mechanisms of PD-1/PD-L1 expression is essential for optimizing cancer immunotherapy in these malignancies (Fig. 4; Table 3).</p><p>Mutational loads across different tumor types correlate with tumor immunogenicity.Reproduced with permission [170].</p><p>The sentences should read:</p><p> Understanding these regulatory mechanisms and identifying new targets for modifying PD-1/PD-L1 are crucial for advancing precise immunotherapies for genitourinary malignancies.</p><p>Therefore, understanding the regulatory mechanisms of PD-1/PD-L1 expression is essential for optimizing cancer immunotherapy in these malignancies (Fig. 5; Table 3).</p><p>Mutational loads across different tumor types correlate with tumor immunogenicity. Reproduced with permission [171].</p><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Liu Q, Guan Y, Li S. Programmed death receptor (PD-)1/PD-ligand (L)1 in urological cancers: the all-around warrior in immunotherapy. Mol Cancer. 2024;23:183. https://doi.org/10.1186/s12943-024-02095-8.</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>Department of Urology, Cancer Hospital of Dalian University of Technology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, 110042, Liaoning, China</p><p>Qiang Liu</p></li><li><p>Second Ward of Bone and Soft Tissue Tumor Surgery, Cancer Hospital of Dalian University of Technology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, 110042, Liaoning, China</p><p>Yujing Guan & Shenglong Li</p></li><li><p>The Liaoning Provincial Key Laboratory of Interdisciplinary Research on Gastrointestinal Tumor Combining Medicine with Engineering, Shenyang, 110042, Liaoning, China</p><p>Yujing Guan & Shenglong Li</p></li><li><p>Institute of Cancer Medicine, Faculty of Medicine, Dalian University of Technology, No.2 Linggong Road, Ganjingzi District, Dalian, 116024, Liaoning Province, China</p><p>Yujing Guan & Shenglong Li</p></li><
更正：Mol Cancer 23, 183 (2024)https://doi.org/10.1186/s12943-024-02095-8Following 原文[1]发表后，作者报告说已发表的PDF版本中的"（见图5）"、"（图4；表3）"和"[170]"等信息有误，需要删除并相应更新，如下所示。原文已经更正：因此，了解 PD-1/PD-L1 表达的调控机制对于优化这些恶性肿瘤的癌症免疫疗法至关重要（图 4；表 3）。不同肿瘤类型的突变负荷与肿瘤免疫原性相关：因此，了解 PD-1/PD-L1 表达的调控机制对于优化这些恶性肿瘤的癌症免疫疗法至关重要（图 5；表 3）。不同肿瘤类型的突变负荷与肿瘤免疫原性相关。Liu Q, Guan Y, Li S. Programmed death receptor (PD-)1/PD-ligand (L)1 in urlogical cancers: the all-around warrior in immunotherapy.Mol Cancer.2024;23:183. https://doi.org/10.1186/s12943-024-02095-8.Article PubMed PubMed Central Google Scholar Download references作者及单位大连理工大学附属肿瘤医院、中国医科大学附属肿瘤医院、辽宁省肿瘤医院暨研究所泌尿外科，辽宁沈阳，110042刘强大连理工大学附属肿瘤医院、中国医科大学附属肿瘤医院、辽宁省肿瘤医院暨研究所骨与软组织肿瘤外科二病区，辽宁沈阳，110042；辽宁省胃肠道肿瘤医工结合交叉研究省级重点实验室，辽宁沈阳，110042 关玉晶、李胜龙大连理工大学医学院肿瘤研究所，辽宁沈阳，1100422辽宁省大连市甘井子区凌工路 2 号大连理工大学医学院肿瘤医学研究所，辽宁省大连市甘井子区凌工路 2 号，116024 关玉晶 & 李胜龙作者简介Qiang Liu查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者关玉晶查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者李胜龙查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者通讯作者：李胜龙。出版者注释Springer Nature对出版地图中的管辖权主张和机构隶属关系保持中立。原文的在线版本可在 https://doi.org/10.1186/s12943-024-02095-8.Open Access 上找到。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 articleLiu, Q., Guan, Y. & Li, S. Correction：泌尿系统癌症中的程序性死亡受体（PD-）1/PD-配体（L）1：免疫疗法中的 "全能战士"。Mol Cancer 23, 199 (2024). https://doi.org/10.1186/s12943-024-02121-9Download citationPublished: 14 September 2024DOI: https://doi.org/10.1186/s12943-024-02121-9Share 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: Programmed death receptor (PD-)1/PD-ligand (L)1 in urological cancers: the “all-around warrior” in immunotherapy","authors":"Qiang Liu, Yujing Guan, Shenglong Li","doi":"10.1186/s12943-024-02121-9","DOIUrl":"https://doi.org/10.1186/s12943-024-02121-9","url":null,"abstract":"<p><b>Correction: Mol Cancer 23, 183 (2024)</b></p><p><b>https://doi.org/10.1186/s12943-024-02095-8</b></p><p>Following publication of the original article [1], the author reported that the published PDF version is incorrect as the information such as “(See Fig. 5)”, “(Fig. 4; Table 3)”, and “[170]” need to be removed and updated accordingly as shown below. The original article has been corrected.</p><p>The sentences currently read:</p><p> Understanding these regulatory mechanisms and identifying new targets for modifying PD-1/PD-L1 are crucial for advancing precise immunotherapies for genitourinary malignancies (See Fig. 5).</p><p>Therefore, understanding the regulatory mechanisms of PD-1/PD-L1 expression is essential for optimizing cancer immunotherapy in these malignancies (Fig. 4; Table 3).</p><p>Mutational loads across different tumor types correlate with tumor immunogenicity.Reproduced with permission [170].</p><p>The sentences should read:</p><p> Understanding these regulatory mechanisms and identifying new targets for modifying PD-1/PD-L1 are crucial for advancing precise immunotherapies for genitourinary malignancies.</p><p>Therefore, understanding the regulatory mechanisms of PD-1/PD-L1 expression is essential for optimizing cancer immunotherapy in these malignancies (Fig. 5; Table 3).</p><p>Mutational loads across different tumor types correlate with tumor immunogenicity. Reproduced with permission [171].</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Liu Q, Guan Y, Li S. Programmed death receptor (PD-)1/PD-ligand (L)1 in urological cancers: the all-around warrior in immunotherapy. Mol Cancer. 2024;23:183. https://doi.org/10.1186/s12943-024-02095-8.</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>Department of Urology, Cancer Hospital of Dalian University of Technology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, 110042, Liaoning, China</p><p>Qiang Liu</p></li><li><p>Second Ward of Bone and Soft Tissue Tumor Surgery, Cancer Hospital of Dalian University of Technology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, 110042, Liaoning, China</p><p>Yujing Guan & Shenglong Li</p></li><li><p>The Liaoning Provincial Key Laboratory of Interdisciplinary Research on Gastrointestinal Tumor Combining Medicine with Engineering, Shenyang, 110042, Liaoning, China</p><p>Yujing Guan & Shenglong Li</p></li><li><p>Institute of Cancer Medicine, Faculty of Medicine, Dalian University of Technology, No.2 Linggong Road, Ganjingzi District, Dalian, 116024, Liaoning Province, China</p><p>Yujing Guan & Shenglong Li</p></li><","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"27 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142231295","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 : 2024-09-13DOI: 10.1186/s12943-024-02092-x
Sophie Cousin, Jean-Philippe Guégan, Kohei Shitara, Lola Jade Palmieri, Jean Philippe Metges, Simon Pernot, Shota Fukuoka, Shohei Koyama, Hiroyoshi Nishikawa, Carine A. Bellera, Antoine Adenis, Carlos A. Gomez-Roca, Philippe Alexandre Cassier, Antoine Hollebecque, Coralie Cantarel, Michèle Kind, Isabelle Soubeyran, Lucile Vanhersecke, Alban Bessede, Antoine Italiano
Anti-angiogenic agents elicit considerable immune modulatory effects within the tumor microenvironment, underscoring the rationale for synergistic clinical development of VEGF and immune checkpoint inhibitors in advanced gastric cancer (AGC). Early phase studies involving Asian patients demonstrated encouraging anti-tumor efficacies. We report the results of the REGOMUNE phase II study, in which Caucasian patients were administered regorafenib, a multi-tyrosine kinase inhibitor, in combination with avelumab, a PD-L1-targeting monoclonal antibody. This therapeutic regimen resulted in deep and durable responses in 19% of patients, with the median duration of response not yet reached. Notwithstanding, a significant proportion of AGC patients exhibited no therapeutic advantage, prompting investigations into mechanisms of inherent resistance. Comprehensive biomarker profiling elucidated that non-responders predominantly exhibited an augmented presence of M2 macrophages within the tumor microenvironment and a marked overexpression of S100A10 by neoplastic cells, a protein previously implicated in macrophage chemotaxis. Additionally, peripheral biomarker assessments identified elevated levels of cytokines, including CSF-1, IL-4, IL-8, and TWEAK, correlating with adverse clinical outcomes, thereby accentuating the role of macrophage infiltration in mediating resistance. These insights furnish an invaluable foundation for elucidating, and potentially circumventing, resistance mechanisms in current AGC therapeutic paradigms, emphasizing the integral role of tumor microenvironmental dynamics and immune modulation.
{"title":"Identification of microenvironment features associated with primary resistance to anti-PD-1/PD-L1 + antiangiogenesis in gastric cancer through spatial transcriptomics and plasma proteomics","authors":"Sophie Cousin, Jean-Philippe Guégan, Kohei Shitara, Lola Jade Palmieri, Jean Philippe Metges, Simon Pernot, Shota Fukuoka, Shohei Koyama, Hiroyoshi Nishikawa, Carine A. Bellera, Antoine Adenis, Carlos A. Gomez-Roca, Philippe Alexandre Cassier, Antoine Hollebecque, Coralie Cantarel, Michèle Kind, Isabelle Soubeyran, Lucile Vanhersecke, Alban Bessede, Antoine Italiano","doi":"10.1186/s12943-024-02092-x","DOIUrl":"https://doi.org/10.1186/s12943-024-02092-x","url":null,"abstract":"Anti-angiogenic agents elicit considerable immune modulatory effects within the tumor microenvironment, underscoring the rationale for synergistic clinical development of VEGF and immune checkpoint inhibitors in advanced gastric cancer (AGC). Early phase studies involving Asian patients demonstrated encouraging anti-tumor efficacies. We report the results of the REGOMUNE phase II study, in which Caucasian patients were administered regorafenib, a multi-tyrosine kinase inhibitor, in combination with avelumab, a PD-L1-targeting monoclonal antibody. This therapeutic regimen resulted in deep and durable responses in 19% of patients, with the median duration of response not yet reached. Notwithstanding, a significant proportion of AGC patients exhibited no therapeutic advantage, prompting investigations into mechanisms of inherent resistance. Comprehensive biomarker profiling elucidated that non-responders predominantly exhibited an augmented presence of M2 macrophages within the tumor microenvironment and a marked overexpression of S100A10 by neoplastic cells, a protein previously implicated in macrophage chemotaxis. Additionally, peripheral biomarker assessments identified elevated levels of cytokines, including CSF-1, IL-4, IL-8, and TWEAK, correlating with adverse clinical outcomes, thereby accentuating the role of macrophage infiltration in mediating resistance. These insights furnish an invaluable foundation for elucidating, and potentially circumventing, resistance mechanisms in current AGC therapeutic paradigms, emphasizing the integral role of tumor microenvironmental dynamics and immune modulation.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"29 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142174494","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 : 2024-09-13DOI: 10.1186/s12943-024-02116-6
Jiahui Zhang, Dan Yu, Cheng Ji, Maoye Wang, Min Fu, Yu Qian, Xiaoxin Zhang, Runbi Ji, Chong Li, Jianmei Gu, Xu Zhang
Tumor cells remodel the phenotype and function of tumor microenvironment (TME) cells to favor tumor progression. Previous studies have shown that neutrophils in TME are polarized to N2 tumor-associated neutrophils (TANs) by tumor derived factors, thus promoting tumor growth and metastasis, angiogenesis, therapy resistance, and immunosuppression. Exosomes act as critical intercellular messengers in human health and diseases including cancer. So far, the biological roles of exosomes from N2 TANs in gastric cancer have not been well characterized. Herein, we represented the first report that exosomes from N2 TANs promoted gastric cancer metastasis in vitro and in vivo. We found that exosomes from N2 TANs transferred miR-4745-5p/3911 to gastric cancer cells to downregulate SLIT2 (slit guidance ligand 2) gene expression. Adenovirus-mediated overexpression of SLIT2 reversed the promotion of gastric cancer metastasis by N2 TANs derived exosomes. We further revealed that gastric cancer cells induced glucose metabolic reprogramming in neutrophils through exosomal HMGB1 (high mobility group protein B1)/NF-κB pathway, which mediated neutrophil N2 polarization and miR-4745-5p/3911 upregulation. We further employed ddPCR (droplet digital PCR) to detect the expression of miR-4745-5p/3911 in N2 TANs exosomes from human serum samples and found their increased levels in gastric cancer patients compared to healthy controls and benign gastric disease patients. Conclusively, our results indicate that N2 TANs facilitate cancer metastasis via regulation of SLIT2 in gastric cancer cells by exosomal miR-4745-5p/3911, which provides a new insight into the roles of TME cells derived exosomes in gastric cancer metastasis and offers a potential biomarker for gastric cancer diagnosis.
肿瘤细胞重塑了肿瘤微环境（TME）细胞的表型和功能，从而有利于肿瘤的进展。以往的研究表明，肿瘤微环境中的中性粒细胞在肿瘤衍生因子的作用下极化为N2肿瘤相关中性粒细胞（TANs），从而促进肿瘤生长和转移、血管生成、抗药性和免疫抑制。外泌体在人类健康和疾病（包括癌症）中扮演着重要的细胞间信使角色。迄今为止，N2 TANs 外泌体在胃癌中的生物学作用尚未得到很好的表征。在本文中，我们首次报道了来自 N2 TANs 的外泌体促进了胃癌的体外和体内转移。我们发现，N2 TANs的外泌体将miR-4745-5p/3911转移到胃癌细胞中，从而下调SLIT2（裂隙引导配体2）基因的表达。腺病毒介导的SLIT2过表达逆转了N2 TANs外泌体对胃癌转移的促进作用。我们进一步发现，胃癌细胞通过外泌体 HMGB1（高迁移率基团蛋白 B1）/NF-κB 通路诱导中性粒细胞葡萄糖代谢重编程，从而介导中性粒细胞 N2 极化和 miR-4745-5p/3911 上调。我们进一步利用液滴数字 PCR 检测了人血清样本中 N2 TANs 外泌体中 miR-4745-5p/3911 的表达，结果发现胃癌患者中 miR-4745-5p/3911 的表达水平比健康对照组和良性胃病患者高。最终，我们的研究结果表明，N2 TANs通过外泌体miR-4745-5p/3911调控胃癌细胞中的SLIT2促进癌症转移，这为TME细胞衍生的外泌体在胃癌转移中的作用提供了新的视角，并为胃癌诊断提供了潜在的生物标志物。
{"title":"Exosomal miR-4745-5p/3911 from N2-polarized tumor-associated neutrophils promotes gastric cancer metastasis by regulating SLIT2","authors":"Jiahui Zhang, Dan Yu, Cheng Ji, Maoye Wang, Min Fu, Yu Qian, Xiaoxin Zhang, Runbi Ji, Chong Li, Jianmei Gu, Xu Zhang","doi":"10.1186/s12943-024-02116-6","DOIUrl":"https://doi.org/10.1186/s12943-024-02116-6","url":null,"abstract":"Tumor cells remodel the phenotype and function of tumor microenvironment (TME) cells to favor tumor progression. Previous studies have shown that neutrophils in TME are polarized to N2 tumor-associated neutrophils (TANs) by tumor derived factors, thus promoting tumor growth and metastasis, angiogenesis, therapy resistance, and immunosuppression. Exosomes act as critical intercellular messengers in human health and diseases including cancer. So far, the biological roles of exosomes from N2 TANs in gastric cancer have not been well characterized. Herein, we represented the first report that exosomes from N2 TANs promoted gastric cancer metastasis in vitro and in vivo. We found that exosomes from N2 TANs transferred miR-4745-5p/3911 to gastric cancer cells to downregulate SLIT2 (slit guidance ligand 2) gene expression. Adenovirus-mediated overexpression of SLIT2 reversed the promotion of gastric cancer metastasis by N2 TANs derived exosomes. We further revealed that gastric cancer cells induced glucose metabolic reprogramming in neutrophils through exosomal HMGB1 (high mobility group protein B1)/NF-κB pathway, which mediated neutrophil N2 polarization and miR-4745-5p/3911 upregulation. We further employed ddPCR (droplet digital PCR) to detect the expression of miR-4745-5p/3911 in N2 TANs exosomes from human serum samples and found their increased levels in gastric cancer patients compared to healthy controls and benign gastric disease patients. Conclusively, our results indicate that N2 TANs facilitate cancer metastasis via regulation of SLIT2 in gastric cancer cells by exosomal miR-4745-5p/3911, which provides a new insight into the roles of TME cells derived exosomes in gastric cancer metastasis and offers a potential biomarker for gastric cancer diagnosis.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"17 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142174493","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}
Colitis-associated colorectal cancer (CAC) frequently develops in patients with inflammatory bowel disease (IBD) who have been exposed to a prolonged state of chronic inflammation. The investigation of pharmacological agents and their mechanisms to prevent precancerous lesions and inhibit their progression remains a significant focus and challenge in CAC research. Previous studies have demonstrated that vitexin effectively mitigates CAC, however, its precise mechanism of action warrants further exploration. This study reveals that the absence of the Vitamin D receptor (VDR) accelerates the progression from chronic colitis to colorectal cancer. Our findings indicate that vitexin can specifically target the VDR protein, facilitating its translocation into the cell nucleus to exert transcriptional activity. Additionally, through a co-culture model of macrophages and cancer cells, we observed that vitexin promotes the polarization of macrophages towards the M1 phenotype, a process that is dependent on VDR. Furthermore, ChIP-seq analysis revealed that vitexin regulates the transcriptional activation of phenazine biosynthesis-like domain protein (PBLD) via VDR. ChIP assays and dual luciferase reporter assays were employed to identify the functional PBLD regulatory region, confirming that the VDR/PBLD pathway is critical for vitexin-mediated regulation of macrophage polarization. Finally, in a mouse model with myeloid VDR gene knockout, we found that the protective effects of vitexin were abolished in mid-stage CAC. In summary, our study establishes that vitexin targets VDR and modulates macrophage polarization through the VDR/PBLD pathway, thereby alleviating the transition from chronic colitis to colorectal cancer.
{"title":"Discovery of vitexin as a novel VDR agonist that mitigates the transition from chronic intestinal inflammation to colorectal cancer","authors":"Yonger Chen, Jian Liang, Shuxian Chen, Nan Lin, Shuoxi Xu, Jindian Miao, Jing Zhang, Chen Chen, Xin Yuan, Zhuoya Xie, Enlin Zhu, Mingsheng Cai, Xiaoli Wei, Shaozhen Hou, Hailin Tang","doi":"10.1186/s12943-024-02108-6","DOIUrl":"https://doi.org/10.1186/s12943-024-02108-6","url":null,"abstract":" Colitis-associated colorectal cancer (CAC) frequently develops in patients with inflammatory bowel disease (IBD) who have been exposed to a prolonged state of chronic inflammation. The investigation of pharmacological agents and their mechanisms to prevent precancerous lesions and inhibit their progression remains a significant focus and challenge in CAC research. Previous studies have demonstrated that vitexin effectively mitigates CAC, however, its precise mechanism of action warrants further exploration. This study reveals that the absence of the Vitamin D receptor (VDR) accelerates the progression from chronic colitis to colorectal cancer. Our findings indicate that vitexin can specifically target the VDR protein, facilitating its translocation into the cell nucleus to exert transcriptional activity. Additionally, through a co-culture model of macrophages and cancer cells, we observed that vitexin promotes the polarization of macrophages towards the M1 phenotype, a process that is dependent on VDR. Furthermore, ChIP-seq analysis revealed that vitexin regulates the transcriptional activation of phenazine biosynthesis-like domain protein (PBLD) via VDR. ChIP assays and dual luciferase reporter assays were employed to identify the functional PBLD regulatory region, confirming that the VDR/PBLD pathway is critical for vitexin-mediated regulation of macrophage polarization. Finally, in a mouse model with myeloid VDR gene knockout, we found that the protective effects of vitexin were abolished in mid-stage CAC. In summary, our study establishes that vitexin targets VDR and modulates macrophage polarization through the VDR/PBLD pathway, thereby alleviating the transition from chronic colitis to colorectal cancer. ","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"63 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142174528","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 : 2024-09-12DOI: 10.1186/s12943-024-02111-x
Min Kang, Bo Tang, Jixi Li, Ziyan Zhou, Kang Liu, Rensheng Wang, Ziyan Jiang, Fangfang Bi, David Patrick, Dongin Kim, Anirban K. Mitra, Yang Yang-Hartwich
<p><b>Correction: Mol Cancer 19, 143 (2020)</b></p><p><b>https://doi.org/10.1186/s12943-020-01248-9</b></p><p>Recently in a re-examination of our previously published paper [1], “Identification of miPEP133 as a novel tumor-suppressor microprotein encoded by miR-34a pri-miRNA” [Molecular Cancer 19, article number 143 (2020)], we found two errors.</p><p>The first error is that we presented the wrong primer sequences for GAPDH in the Supplemental Methods (in the Additional file 2). We mistakenly listed the primer sequences for human β-actin (<i>ACTB</i>) as for GAPDH. The correct primer sequences for GAPDH are 5′-AATGAAGGGGTCATTGATGG − 3′ and 5′-AAGGTGAAGGTCGGAGTCAA − 3′. These were used in this study. Please find the resized Additional file 2 in the attachment.</p><p>The other error is a misplaced western blot image for the loading control β-actin in Fig. 4e. We have identified the correct image for β-actin bands. The following is the corrected figure.</p><figure><picture><img alt="figure a" aria-describedby="Figa" height="889" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02111-x/MediaObjects/12943_2024_2111_Fig1_HTML.png" width="685"/></picture></figure><p>They are minor errors, and their correction does not affect the conclusion of this article, however, we sincerely apologize to the readers and editors for the inconvenience caused by our mistakes. We would like to ask for an opportunity to publish this correction.</p><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Kang M, Tang B, Li J, et al. Identification of miPEP133 as a novel tumor-suppressor microprotein encoded by miR-34a pri-miRNA. Mol Cancer. 2020;19:143. https://doi.org/10.1186/s12943-020-01248-9.</p><p>Article CAS 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>The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530022, China</p><p>Min Kang, Bo Tang, Jixi Li, Ziyan Zhou & Kang Liu</p></li><li><p>Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, CT, 06510, USA</p><p>Min Kang, Ziyan Jiang, Fangfang Bi, David Patrick & Yang Yang-Hartwich</p></li><li><p>Department of Radiation Oncology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530021, China</p><p>Min Kang & Rensheng Wang</p></li><li><p>Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530021, China</p><p>Bo Tang</p></li><li><p>The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210029, China</p><p>Ziyan Jiang</p></li><li><p>Sheng Jing Hospital of China Medical
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中，除非在材料的信用栏中另有说明。如果文章中的材料未包含在知识共享许可协议中，并且您的使用意图未得到法律法规的许可或超出了许可使用范围，您需要直接从版权所有者处获得许可。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 articleKang, M., Tang, B., Li, J. et al. Correction：miR-34a pri-miRNA编码的新型肿瘤抑制微蛋白miPEP133的鉴定。Mol Cancer 23, 195 (2024). https://doi.org/10.1186/s12943-024-02111-xDownload citationPublished: 12 September 2024DOI: https://doi.org/10.1186/s12943-024-02111-xShare 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 miPEP133 as a novel tumor-suppressor microprotein encoded by miR-34a pri-miRNA","authors":"Min Kang, Bo Tang, Jixi Li, Ziyan Zhou, Kang Liu, Rensheng Wang, Ziyan Jiang, Fangfang Bi, David Patrick, Dongin Kim, Anirban K. Mitra, Yang Yang-Hartwich","doi":"10.1186/s12943-024-02111-x","DOIUrl":"https://doi.org/10.1186/s12943-024-02111-x","url":null,"abstract":"<p><b>Correction: Mol Cancer 19, 143 (2020)</b></p><p><b>https://doi.org/10.1186/s12943-020-01248-9</b></p><p>Recently in a re-examination of our previously published paper [1], “Identification of miPEP133 as a novel tumor-suppressor microprotein encoded by miR-34a pri-miRNA” [Molecular Cancer 19, article number 143 (2020)], we found two errors.</p><p>The first error is that we presented the wrong primer sequences for GAPDH in the Supplemental Methods (in the Additional file 2). We mistakenly listed the primer sequences for human β-actin (<i>ACTB</i>) as for GAPDH. The correct primer sequences for GAPDH are 5′-AATGAAGGGGTCATTGATGG − 3′ and 5′-AAGGTGAAGGTCGGAGTCAA − 3′. These were used in this study. Please find the resized Additional file 2 in the attachment.</p><p>The other error is a misplaced western blot image for the loading control β-actin in Fig. 4e. We have identified the correct image for β-actin bands. The following is the corrected figure.</p><figure><picture><img alt=\"figure a\" aria-describedby=\"Figa\" height=\"889\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02111-x/MediaObjects/12943_2024_2111_Fig1_HTML.png\" width=\"685\"/></picture></figure><p>They are minor errors, and their correction does not affect the conclusion of this article, however, we sincerely apologize to the readers and editors for the inconvenience caused by our mistakes. We would like to ask for an opportunity to publish this correction.</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Kang M, Tang B, Li J, et al. Identification of miPEP133 as a novel tumor-suppressor microprotein encoded by miR-34a pri-miRNA. Mol Cancer. 2020;19:143. https://doi.org/10.1186/s12943-020-01248-9.</p><p>Article CAS 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>The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530022, China</p><p>Min Kang, Bo Tang, Jixi Li, Ziyan Zhou & Kang Liu</p></li><li><p>Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, CT, 06510, USA</p><p>Min Kang, Ziyan Jiang, Fangfang Bi, David Patrick & Yang Yang-Hartwich</p></li><li><p>Department of Radiation Oncology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530021, China</p><p>Min Kang & Rensheng Wang</p></li><li><p>Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530021, China</p><p>Bo Tang</p></li><li><p>The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210029, China</p><p>Ziyan Jiang</p></li><li><p>Sheng Jing Hospital of China Medical","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"57 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142170752","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 : 2024-09-11DOI: 10.1186/s12943-024-02112-w
Qing Shi, Yasheng Zhu, Jian Ma, Kun Chang, Dongling Ding, Yang Bai, Kun Gao, Pingzhao Zhang, Ren Mo, Kai Feng, Xiaying Zhao, Liang Zhang, Huiru Sun, Dongyue Jiao, Yingji Chen, Yinghao Sun, Shi-min Zhao, Haojie Huang, Yao Li, Shancheng Ren, Chenji Wang
<p><b>Correction</b><b>: </b><b>Mol Cancer 18, 170 (2019)</b></p><p><b>https://doi.org/10.1186/s12943-019-1096-x</b></p><br/><p>The authors apologize for the errors in Fig. 2. In the original published version [1], the western blot image of Actin in Fig. 2D was mistakenly uploaded. The Western blot image of BRD4 in Fig. 2G was mistakenly uploaded. The Western blot one lane of FLAG (Input) in Fig. 2K was inadvertently omitted due to a careless mistake. The correct figure is shown below.</p><figure><picture><source srcset="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02112-w/MediaObjects/12943_2024_2112_Figa_HTML.png?as=webp" type="image/webp"/><img alt="figure a" aria-describedby="Figa" height="544" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02112-w/MediaObjects/12943_2024_2112_Figa_HTML.png" width="685"/></picture></figure><p>The authors apologize for the errors in Fig. 3. In the original published version, the Western blot image of Myc (Input) in Fig. 3A was mistakenly uploaded. The Western blot image of Myc (Input) in Fig. 3C was mistakenly uploaded. The Western blot image of FLAG in Fig. 3D was mistakenly uploaded. The correct figure is shown below.</p><figure><picture><source srcset="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02112-w/MediaObjects/12943_2024_2112_Figb_HTML.png?as=webp" type="image/webp"/><img alt="figure b" aria-describedby="Figb" height="655" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02112-w/MediaObjects/12943_2024_2112_Figb_HTML.png" width="685"/></picture></figure><p>The authors apologize for two errors in Supplementary Figure 1. In the original published version, the Western blot image of FLAG (Input) in Supplementary Figure 1C was mistakenly uploaded. The Western blot image of FLAG (Input) in Supplementary Figure 1E was mistakenly uploaded. The correct figure is shown below.</p><figure><picture><source srcset="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02112-w/MediaObjects/12943_2024_2112_Figc_HTML.png?as=webp" type="image/webp"/><img alt="figure c" aria-describedby="Figc" height="562" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02112-w/MediaObjects/12943_2024_2112_Figc_HTML.png" width="685"/></picture></figure><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Shi Q, Zhu Y, Ma J, et al. Prostate Cancer-associated SPOP mutations enhance cancer cell survival and docetaxel resistance by upregulating Caprin1-dependent stress granule assembly. Mol Cancer. 2019;18:170. https://doi.org/10.1186/s12943-019-1096-x.</p><p>Article CAS PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use x
更正：Mol Cancer 18, 170 (2019)https://doi.org/10.1186/s12943-019-1096-xThe 作者对图2中的错误表示歉意。在最初发表的版本[1]中，图2D中Actin的Western印迹图像被错误上传。图 2G 中 BRD4 的 Western 印迹图像上传有误。由于粗心大意，图 2K 中的 FLAG（输入）Western 印迹单道图像被误删。作者对图 3 中的错误表示歉意。在最初发表的版本中，图 3A 中 Myc（输入）的 Western 印迹图像被错误上传。图 3C 中 Myc（输入）的 Western 印迹图像被错误上传。图 3D 中 FLAG 的 Western 印迹图像上传错误。作者对补充图 1 中的两处错误表示歉意。在最初发表的版本中，补图 1C 中 FLAG（输入）的 Western 印迹图像被错误上传。补充图 1E 中 FLAG（输入）的 Western 印迹图像被错误上传。Shi Q, Zhu Y, Ma J, et al. Prostate Cancer-associated SPOP mutations enhance cancer cell survival and docetaxel resistance by upregulating Caprin1-dependent stress granule assembly.Mol Cancer.2019;18:170. https://doi.org/10.1186/s12943-019-1096-x.Article CAS PubMed PubMed Central Google Scholar Download references作者注释石青、朱亚圣和马健对本研究做出了同样的贡献。
{"title":"Correction: Prostate cancer-associated SPOP mutations enhance cancer cell survival and docetaxel resistance by upregulating Caprin1-dependent stress granule assembly","authors":"Qing Shi, Yasheng Zhu, Jian Ma, Kun Chang, Dongling Ding, Yang Bai, Kun Gao, Pingzhao Zhang, Ren Mo, Kai Feng, Xiaying Zhao, Liang Zhang, Huiru Sun, Dongyue Jiao, Yingji Chen, Yinghao Sun, Shi-min Zhao, Haojie Huang, Yao Li, Shancheng Ren, Chenji Wang","doi":"10.1186/s12943-024-02112-w","DOIUrl":"https://doi.org/10.1186/s12943-024-02112-w","url":null,"abstract":"<p><b>Correction</b><b>: </b><b>Mol Cancer 18, 170 (2019)</b></p><p><b>https://doi.org/10.1186/s12943-019-1096-x</b></p><br/><p>The authors apologize for the errors in Fig. 2. In the original published version [1], the western blot image of Actin in Fig. 2D was mistakenly uploaded. The Western blot image of BRD4 in Fig. 2G was mistakenly uploaded. The Western blot one lane of FLAG (Input) in Fig. 2K was inadvertently omitted due to a careless mistake. The correct figure is shown below.</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02112-w/MediaObjects/12943_2024_2112_Figa_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure a\" aria-describedby=\"Figa\" height=\"544\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02112-w/MediaObjects/12943_2024_2112_Figa_HTML.png\" width=\"685\"/></picture></figure><p>The authors apologize for the errors in Fig. 3. In the original published version, the Western blot image of Myc (Input) in Fig. 3A was mistakenly uploaded. The Western blot image of Myc (Input) in Fig. 3C was mistakenly uploaded. The Western blot image of FLAG in Fig. 3D was mistakenly uploaded. The correct figure is shown below.</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02112-w/MediaObjects/12943_2024_2112_Figb_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure b\" aria-describedby=\"Figb\" height=\"655\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02112-w/MediaObjects/12943_2024_2112_Figb_HTML.png\" width=\"685\"/></picture></figure><p>The authors apologize for two errors in Supplementary Figure 1. In the original published version, the Western blot image of FLAG (Input) in Supplementary Figure 1C was mistakenly uploaded. The Western blot image of FLAG (Input) in Supplementary Figure 1E was mistakenly uploaded. The correct figure is shown below.</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02112-w/MediaObjects/12943_2024_2112_Figc_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure c\" aria-describedby=\"Figc\" height=\"562\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-024-02112-w/MediaObjects/12943_2024_2112_Figc_HTML.png\" width=\"685\"/></picture></figure><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Shi Q, Zhu Y, Ma J, et al. Prostate Cancer-associated SPOP mutations enhance cancer cell survival and docetaxel resistance by upregulating Caprin1-dependent stress granule assembly. Mol Cancer. 2019;18:170. https://doi.org/10.1186/s12943-019-1096-x.</p><p>Article CAS PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use x","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"43 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142166195","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}
CD8+ T cells are the workhorses executing adaptive anti-tumour response, and targets of various cancer immunotherapies. Latest advances have unearthed the sheer heterogeneity of CD8+ tumour infiltrating lymphocytes, and made it increasingly clear that the bulk of the endogenous and therapeutically induced tumour-suppressive momentum hinges on a particular selection of CD8+ T cells with advantageous attributes, namely the memory and stem-like exhausted subsets. A scrutiny of the contemporary perception of CD8+ T cells in cancer and the subgroups of interest along with the factors arbitrating their infiltration contextures, presented herein, may serve as the groundwork for future endeavours to probe further into the regulatory networks underlying their differentiation and migration, and optimise T cell-based immunotherapies accordingly.
CD8+ T 细胞是执行适应性抗肿瘤反应的主力军，也是各种癌症免疫疗法的靶点。最新进展揭示了 CD8+ 肿瘤浸润淋巴细胞的纯粹异质性，并使人们越来越清楚地认识到，大部分内源性和治疗性诱导的肿瘤抑制动力取决于具有优势属性的特定 CD8+ T 细胞选择，即记忆和干样衰竭亚群。本文对CD8+ T细胞在癌症中的当代认知、相关亚群以及决定其浸润环境的因素进行了仔细研究，为今后进一步探究CD8+ T细胞分化和迁移的基础调控网络并相应优化基于T细胞的免疫疗法奠定了基础。
{"title":"Phenotypic and spatial heterogeneity of CD8+ tumour infiltrating lymphocytes","authors":"Yikan Sun, Eloy Yinwang, Shengdong Wang, Zenan Wang, Fangqian Wang, Yucheng Xue, Wenkan Zhang, Shenzhi Zhao, Haochen Mou, Shixin Chen, Lingxiao Jin, Binghao Li, Zhaoming Ye","doi":"10.1186/s12943-024-02104-w","DOIUrl":"https://doi.org/10.1186/s12943-024-02104-w","url":null,"abstract":"CD8+ T cells are the workhorses executing adaptive anti-tumour response, and targets of various cancer immunotherapies. Latest advances have unearthed the sheer heterogeneity of CD8+ tumour infiltrating lymphocytes, and made it increasingly clear that the bulk of the endogenous and therapeutically induced tumour-suppressive momentum hinges on a particular selection of CD8+ T cells with advantageous attributes, namely the memory and stem-like exhausted subsets. A scrutiny of the contemporary perception of CD8+ T cells in cancer and the subgroups of interest along with the factors arbitrating their infiltration contextures, presented herein, may serve as the groundwork for future endeavours to probe further into the regulatory networks underlying their differentiation and migration, and optimise T cell-based immunotherapies accordingly.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"1 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142158812","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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