Pub Date : 2024-09-18DOI: 10.1186/s12935-024-03505-z
Guixin Wang, Cangchang Shi, Long He, Yingxi Li, Wenbin Song, Zhaohui Chen, Zhaoyi Liu, Yizeng Wang, Xianghui He, Yue Yu, Yao Tian, Xin Wang
Tumor metastasis is a continuous and dynamic process and is a major cause of tumor-related death in triple-negative breast cancer. However, this biological process remains largely unknown in triple-negative breast cancer. The emergence of single-cell sequencing enables a deeper understanding of the tumor microenvironment and provides a new strategy for discovering the potential mechanism of tumor metastasis. Herein, we integrated the single-cell expression profiling of primary and metastatic triple-negative breast cancer by Seurat package. Nine tumor cell subgroups were identified. Enrichment analysis suggested tumor subgroups (C0, C4) were associated with tumor metastasis with poor prognosis in TNBC. Weighted gene co-expression network was constructed and identified NENF was a metastasis-related gene. Subsequently, RT-qPCR, Immunohistochemistry, and western blot confirmed NENF is highly expressed in TNBC tissues. And cell function assays indicated NENF promote cell invasion and migration through regulating EMT in TNBC. Finally, TIDE and Connectivity Map database suggest the candidate drugs for targeting NENF. In conclusion, our findings provide a new insight into the progression and metastasis of TNBC and uncover NENF may be a prognostic biomarker and potential therapy targets.
{"title":"Identification of the tumor metastasis-related tumor subgroups overexpressed NENF in triple-negative breast cancer by single-cell transcriptomics","authors":"Guixin Wang, Cangchang Shi, Long He, Yingxi Li, Wenbin Song, Zhaohui Chen, Zhaoyi Liu, Yizeng Wang, Xianghui He, Yue Yu, Yao Tian, Xin Wang","doi":"10.1186/s12935-024-03505-z","DOIUrl":"https://doi.org/10.1186/s12935-024-03505-z","url":null,"abstract":"Tumor metastasis is a continuous and dynamic process and is a major cause of tumor-related death in triple-negative breast cancer. However, this biological process remains largely unknown in triple-negative breast cancer. The emergence of single-cell sequencing enables a deeper understanding of the tumor microenvironment and provides a new strategy for discovering the potential mechanism of tumor metastasis. Herein, we integrated the single-cell expression profiling of primary and metastatic triple-negative breast cancer by Seurat package. Nine tumor cell subgroups were identified. Enrichment analysis suggested tumor subgroups (C0, C4) were associated with tumor metastasis with poor prognosis in TNBC. Weighted gene co-expression network was constructed and identified NENF was a metastasis-related gene. Subsequently, RT-qPCR, Immunohistochemistry, and western blot confirmed NENF is highly expressed in TNBC tissues. And cell function assays indicated NENF promote cell invasion and migration through regulating EMT in TNBC. Finally, TIDE and Connectivity Map database suggest the candidate drugs for targeting NENF. In conclusion, our findings provide a new insight into the progression and metastasis of TNBC and uncover NENF may be a prognostic biomarker and potential therapy targets.","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"20 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142264884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p><b>Cancer Cell International (2020) 20:97</b></p><p><b>https://doi.org/10.1186/s12935-020-01186-y</b>.</p><p><b>Retraction Note</b></p><p>The Editor-in-Chief has retracted this article at the authors’ request. After publication, concerns were raised regarding the data included in the figures. Specifically:</p><ul> <li> <p>Fig. 1e 0 Gy images appear to be assembled incorrectly, and the EdU images for 0.125 and 0.25 µM S109 appear highly similar;</p> </li> <li> <p>Fig. 2c 0.25 µM 6 Gy image appears highly similar to Fig. 1i (C6 cells, 25 µM GDC-0449) of another article [1] from the same author group;</p> </li> <li> <p>Fig. 4b 0 mg/kg S109 10 Gy Day 10 (2nd mouse) and Day 18 (2nd mouse) images appear highly similar;</p> </li> <li> <p>Fig. 4e 0 mg/kg S109 10 Gy and 50 mg/kg S109 0 Gy images appear to overlap.</p> </li> </ul><p>The authors have stated that incorrect images were included in the figure panels during figure preparation. Although the authors believe that these issues do not affect the conclusions of the study, they requested to retract the article to prevent any potential confusion or misinterpretation by readers.</p><p>Xuejiao Liu stated on behalf of all authors that all authors agree to this retraction.</p><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Tu Y, Niu M, Xie P, et al. Smoothened is a poor prognosis factor and a potential therapeutic target in glioma. Sci Rep. 2017;7:42630. https://doi.org/10.1038/srep42630.</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>Insititute of Nervous System Diseases, Affiliated Hospital of Xuzhou Medical University, Xuzhou Medical University, Xuzhou, Jiangsu, China</p><p>Xuejiao Liu, Yiming Tu, Yifeng Wang, Di Zhou, Lin Shi, Guanzheng Liu, Xu Zhang, Huan Li, Shangfeng Gao, Mingshan Niu & Rutong Yu</p></li><li><p>Department of Neurosurgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China</p><p>Xuejiao Liu, Xu Zhang, Shangfeng Gao & Rutong Yu</p></li><li><p>Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China</p><p>Yiming Tu</p></li><li><p>Department of Neurosurgery, Suqian Hospital Affiliated to Xuzhou Medical University, Suqian, Jiangsu, China</p><p>Yulong Chong</p></li><li><p>College of Pharmacy, The Ohio State University, Columbus, OH, USA</p><p>Sijin Wu</p></li><li><p>Blood Diseases Institute, Xuzhou Medical University, Xuzhou, Jiangsu, China</p><p>Mingshan Niu</p></li></ol><span>Authors</span><ol><li><span>Xuejiao 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>Yiming Tu</span>View author publications<p>You can also search for this author
1186/s12935-024-03508-wDownload citationAccepted:13 September 2024Published: 18 September 2024DOI: https://doi.org/10.1186/s12935-024-03508-wShare this articleAnyone you share with the following link 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":"Retraction Note: Reversible inhibitor of CRM1 sensitizes glioblastoma cells to radiation by blocking the NF-κB signaling pathway","authors":"Xuejiao Liu, Yiming Tu, Yifeng Wang, Di Zhou, Yulong Chong, Lin Shi, Guanzheng Liu, Xu Zhang, Sijin Wu, Huan Li, Shangfeng Gao, Mingshan Niu, Rutong Yu","doi":"10.1186/s12935-024-03508-w","DOIUrl":"https://doi.org/10.1186/s12935-024-03508-w","url":null,"abstract":"<p><b>Cancer Cell International (2020) 20:97</b></p><p><b>https://doi.org/10.1186/s12935-020-01186-y</b>.</p><p><b>Retraction Note</b></p><p>The Editor-in-Chief has retracted this article at the authors’ request. After publication, concerns were raised regarding the data included in the figures. Specifically:</p><ul>\u0000<li>\u0000<p>Fig. 1e 0 Gy images appear to be assembled incorrectly, and the EdU images for 0.125 and 0.25 µM S109 appear highly similar;</p>\u0000</li>\u0000<li>\u0000<p>Fig. 2c 0.25 µM 6 Gy image appears highly similar to Fig. 1i (C6 cells, 25 µM GDC-0449) of another article [1] from the same author group;</p>\u0000</li>\u0000<li>\u0000<p>Fig. 4b 0 mg/kg S109 10 Gy Day 10 (2nd mouse) and Day 18 (2nd mouse) images appear highly similar;</p>\u0000</li>\u0000<li>\u0000<p>Fig. 4e 0 mg/kg S109 10 Gy and 50 mg/kg S109 0 Gy images appear to overlap.</p>\u0000</li>\u0000</ul><p>The authors have stated that incorrect images were included in the figure panels during figure preparation. Although the authors believe that these issues do not affect the conclusions of the study, they requested to retract the article to prevent any potential confusion or misinterpretation by readers.</p><p>Xuejiao Liu stated on behalf of all authors that all authors agree to this retraction.</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Tu Y, Niu M, Xie P, et al. Smoothened is a poor prognosis factor and a potential therapeutic target in glioma. Sci Rep. 2017;7:42630. https://doi.org/10.1038/srep42630.</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>Insititute of Nervous System Diseases, Affiliated Hospital of Xuzhou Medical University, Xuzhou Medical University, Xuzhou, Jiangsu, China</p><p>Xuejiao Liu, Yiming Tu, Yifeng Wang, Di Zhou, Lin Shi, Guanzheng Liu, Xu Zhang, Huan Li, Shangfeng Gao, Mingshan Niu & Rutong Yu</p></li><li><p>Department of Neurosurgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China</p><p>Xuejiao Liu, Xu Zhang, Shangfeng Gao & Rutong Yu</p></li><li><p>Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China</p><p>Yiming Tu</p></li><li><p>Department of Neurosurgery, Suqian Hospital Affiliated to Xuzhou Medical University, Suqian, Jiangsu, China</p><p>Yulong Chong</p></li><li><p>College of Pharmacy, The Ohio State University, Columbus, OH, USA</p><p>Sijin Wu</p></li><li><p>Blood Diseases Institute, Xuzhou Medical University, Xuzhou, Jiangsu, China</p><p>Mingshan Niu</p></li></ol><span>Authors</span><ol><li><span>Xuejiao 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>Yiming Tu</span>View author publications<p>You can also search for this author ","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"1 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142264885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<br/><p><b>Correction to: Cancer Cell International (2022) 22:32</b> <b>https://doi.org/10.1186/s12935-021-02434-5</b></p><br/><p>In this article [1], the WB band for mTOR in Fig. 3B and the Control group of T98G cells in Fig. 4A were incorrect. The corrected Figs. 3 and 4 are given below.</p><figure><figcaption><b data-test="figure-caption-text">Fig. 3</b></figcaption><picture><source srcset="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig3_HTML.png?as=webp" type="image/webp"/><img alt="figure 3" aria-describedby="Fig3" height="666" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig3_HTML.png" width="685"/></picture><p>4, 5-Dimethoxycanthin-6-one inhibits the AKT/mTOR and MAPK signaling pathways. <b>A</b> 4, 5-Dimethoxycanthin-6-one inhibition of the AKT/mTOR and MAPK signaling pathways in U251 cells. <b>B</b> 4, 5-Dimethoxycanthin-6-one inhibition of the AKT/mTOR and MAPK signaling pathways in T98G cells. *P < 0.05 compared with the Control group</p><span>Full size image</span><svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use xlink:href="#icon-eds-i-chevron-right-small" xmlns:xlink="http://www.w3.org/1999/xlink"></use></svg></figure><figure><figcaption><b data-test="figure-caption-text">Fig. 4</b></figcaption><picture><source srcset="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig4_HTML.png?as=webp" type="image/webp"/><img alt="figure 4" aria-describedby="Fig4" height="1519" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig4_HTML.png" width="685"/></picture><p>4, 5-Dimethoxycanthin-6-one inhibits cell proliferation. <b>A</b> Cell proliferation detected using the EDU assay. <b>B</b> The migration distance of cells was measured using a wound scratch assay. <b>C</b> Colon numbers were analyzed using a colony formation assay. *P < 0.05 compared with the Control group</p><span>Full size image</span><svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use xlink:href="#icon-eds-i-chevron-right-small" xmlns:xlink="http://www.w3.org/1999/xlink"></use></svg></figure><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Li W, Huang BS, Xiong YY, Yang LJ, Wu LX. 4,5-Dimethoxycanthin-6-one is a novel LSD1 inhibitor that inhibits proliferation of glioblastoma cells and induces apoptosis and pyroptosis. Cancer Cell Int. 2022;22:32. https://doi.org/10.1186/s12935-021-02434-5.</p><p>Article PubMed PubMed Central CAS 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/
更正：Cancer Cell International (2022) 22:32 https://doi.org/10.1186/s12935-021-02434-5In 这篇文章[1]中，图 3B 中 mTOR 的 WB 波段和图 4A 中 T98G 细胞的对照组不正确。图 34，5-二甲氧基黄嘌呤-6-酮抑制 AKT/mTOR 和 MAPK 信号通路。A 4,5-二甲氧基黄嘌呤-6-酮抑制 U251 细胞中的 AKT/mTOR 和 MAPK 信号通路。B 4,5-二甲氧基黄嘌呤-6-酮对 T98G 细胞中 AKT/mTOR 和 MAPK 信号通路的抑制作用。*图 44，5-二甲氧基黄嘌呤-6-酮抑制细胞增殖。A 使用 EDU 检测法检测细胞增殖。B 用伤口划痕法测定细胞的迁移距离。C 利用集落形成试验分析集落数量。与对照组相比，*P < 0.05全图Li W, Huang BS, Xiong YY, Yang LJ, Wu LX.4,5-二甲氧基黄嘌呤-6-酮是一种新型 LSD1 抑制剂，可抑制胶质母细胞瘤细胞增殖并诱导细胞凋亡和热凋亡。Cancer Cell Int. 2022;22:32. https://doi.org/10.1186/s12935-021-02434-5.Article PubMed PubMed Central CAS Google Scholar Download references作者及单位湖南省长沙市湘雅路110号中南大学基础医学院生理学系李伟，黄柏生&；南昌大学第二附属医院神经外科，中国南昌 熊元元长沙市第一医院神经外科，中国长沙中国Li-Jian Yang作者Wei Li查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者Bai-Sheng Huang查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者Yuan-Yuan Xiong查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者Li-Jian Yang查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者Li-Xiang Wu查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者Corresponding authorCorrespondence to Li-Xiang Wu.开放获取 本文采用知识共享署名 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使用、共享、改编、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，并说明是否进行了修改。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，除非在材料的署名栏中另有说明。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许可使用范围，则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/4.0/。除非在数据的信用行中另有说明，否则知识共享公共领域专用免责声明 (http://creativecommons.org/publicdomain/zero/1.0/) 适用于本文提供的数据。转载与许可引用本文Li, W., Huang, BS., Xiong, YY. et al. Correction：4,5-二甲氧基黄嘌呤-6-酮是一种新型 LSD1 抑制剂，可抑制胶质母细胞瘤细胞增殖并诱导细胞凋亡和热凋亡。Cancer Cell Int 24, 317 (2024). https://doi.org/10.1186/s12935-024-03311-7Download citationAccepted: 26 March 2024Published: 14 September 2024DOI: https://doi.org/10.1186/s12935-024-03311-7Share 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: 4,5-Dimethoxycanthin-6-one is a novel LSD1 inhibitor that inhibits proliferation of glioblastoma cells and induces apoptosis and pyroptosis","authors":"Wei Li, Bai-Sheng Huang, Yuan-Yuan Xiong, Li-Jian Yang, Li-Xiang Wu","doi":"10.1186/s12935-024-03311-7","DOIUrl":"https://doi.org/10.1186/s12935-024-03311-7","url":null,"abstract":"<br/><p><b>Correction to: Cancer Cell International (2022) 22:32</b> <b>https://doi.org/10.1186/s12935-021-02434-5</b></p><br/><p>In this article [1], the WB band for mTOR in Fig. 3B and the Control group of T98G cells in Fig. 4A were incorrect. The corrected Figs. 3 and 4 are given below.</p><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 3</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig3_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 3\" aria-describedby=\"Fig3\" height=\"666\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig3_HTML.png\" width=\"685\"/></picture><p>4, 5-Dimethoxycanthin-6-one inhibits the AKT/mTOR and MAPK signaling pathways. <b>A</b> 4, 5-Dimethoxycanthin-6-one inhibition of the AKT/mTOR and MAPK signaling pathways in U251 cells. <b>B</b> 4, 5-Dimethoxycanthin-6-one inhibition of the AKT/mTOR and MAPK signaling pathways in T98G cells. *P < 0.05 compared with the Control group</p><span>Full size image</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 4</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig4_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 4\" aria-describedby=\"Fig4\" height=\"1519\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig4_HTML.png\" width=\"685\"/></picture><p>4, 5-Dimethoxycanthin-6-one inhibits cell proliferation. <b>A</b> Cell proliferation detected using the EDU assay. <b>B</b> The migration distance of cells was measured using a wound scratch assay. <b>C</b> Colon numbers were analyzed using a colony formation assay. *P < 0.05 compared with the Control group</p><span>Full size image</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Li W, Huang BS, Xiong YY, Yang LJ, Wu LX. 4,5-Dimethoxycanthin-6-one is a novel LSD1 inhibitor that inhibits proliferation of glioblastoma cells and induces apoptosis and pyroptosis. Cancer Cell Int. 2022;22:32. https://doi.org/10.1186/s12935-021-02434-5.</p><p>Article PubMed PubMed Central CAS 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/","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"34 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142269199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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/s12935-024-03499-8
Jun Rong, Qifu Wang, Tingzheng Li, Jin Qian, Jinchao Cheng
Glioma is a primary brain tumor that grows quickly, has an unfavorable prognosis, and can spread intracerebrally. Glioma cells rely on glucose as the major energy source, and glycolysis plays a critical role in tumorigenesis and progression. Substrate utilization shifts throughout glioma progression to facilitate energy generation and biomass accumulation. This metabolic reprogramming promotes glioma cell proliferation and metastasis and ultimately decreases the efficacy of conventional treatments. Non-coding RNAs (ncRNAs) are involved in several glucose metabolism pathways during tumor initiation and progression. These RNAs influence cell viability and glucose metabolism by modulating the expression of key genes of the glycolytic pathway. They can directly or indirectly affect glycolysis in glioma cells by influencing the transcription and post-transcriptional regulation of oncogenes and suppressor genes. In this review, we discussed the role of ncRNAs in the metabolic reprogramming of glioma cells and tumor microenvironments and their abnormal expression in the glucometabolic pathway in glioma. In addition, we consolidated the existing theoretical knowledge to facilitate the use of this emerging class of biomarkers as biological indicators and potential therapeutic targets for glioma.
{"title":"Glucose metabolism in glioma: an emerging sight with ncRNAs","authors":"Jun Rong, Qifu Wang, Tingzheng Li, Jin Qian, Jinchao Cheng","doi":"10.1186/s12935-024-03499-8","DOIUrl":"https://doi.org/10.1186/s12935-024-03499-8","url":null,"abstract":"Glioma is a primary brain tumor that grows quickly, has an unfavorable prognosis, and can spread intracerebrally. Glioma cells rely on glucose as the major energy source, and glycolysis plays a critical role in tumorigenesis and progression. Substrate utilization shifts throughout glioma progression to facilitate energy generation and biomass accumulation. This metabolic reprogramming promotes glioma cell proliferation and metastasis and ultimately decreases the efficacy of conventional treatments. Non-coding RNAs (ncRNAs) are involved in several glucose metabolism pathways during tumor initiation and progression. These RNAs influence cell viability and glucose metabolism by modulating the expression of key genes of the glycolytic pathway. They can directly or indirectly affect glycolysis in glioma cells by influencing the transcription and post-transcriptional regulation of oncogenes and suppressor genes. In this review, we discussed the role of ncRNAs in the metabolic reprogramming of glioma cells and tumor microenvironments and their abnormal expression in the glucometabolic pathway in glioma. In addition, we consolidated the existing theoretical knowledge to facilitate the use of this emerging class of biomarkers as biological indicators and potential therapeutic targets for glioma.","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"37 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142203546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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/s12935-024-03489-w
Qi Li, Wenjie Yang, Qingyi Zhang, Daoming Zhang, Jun Deng, Binxin Chen, Ping Li, Huanqi Zhang, Yiming Jiang, Yangling Li, Bo Zhang, Nengming Lin
Lung squamous cell carcinoma (LUSCs) is associated with high mortality (20–30%) and lacks of effective treatments. Almost all LUSC exhibit somatic mutations in TP53. Wee1, a tyrosine kinase, regulates the cell cycle at the G2/M checkpoint. In TP53-deficient cells, the dependence on G2/M checkpoints increases. PD0166285 is the first reported drug with inhibitory activity against both Wee1 and PKMYT1. Protein expression was determined by Western blot analysis. Cell proliferation was assessed using cell colony formation and CCK-8 assays. Cell cycle was performed by PI staining with flow cytometry. Apoptosis was evaluated using Annexin V-Phycoerythrin double staining and flow cytometry. DNA damage was detected through comet assay and immunofluorescence assay. In vivo, apoptosis and anti-tumor effects were assessed using the TUNEL assay, a nude mouse model, and immunohistochemistry (IHC). Co-immunoprecipitation assay was used to detect protein–protein interactions. We analyzed Wee1, PKMYT1, and Stat1 expression in pan-cancer studies using the Ualcan public database and assessed their prognostic implications with Kaplan–Meier curves. PD0166285, a Wee1 inhibitor, effectively inhibits Wee1 activity, promoting cell entry into a mitotic crisis. Moreover, PD0166285 sensitizes cells to cisplatin, enhancing clinical outcomes. Our study demonstrated that PD016628 regulates the cell cycle through Rad51 and results in cell cycle arrest at the G2/M phase. We observed increased apoptosis in tumor cells treated with PD0166285, particularly when combined with cisplatin, indicating an enhanced apoptotic response. The upregulation of γ-H2AX serves as an indicator of mitotic catastrophe. Co-immunoprecipitation and data analysis revealed that apoptosis in LUSC is mediated through the Stat1 pathway, accompanied by decreased levels of Socs3. Furthermore, IHC staining confirmed significant differences in the expression of Phospho-CDK1 and γ-H2AX in LUSCs, suggesting involvement in DNA damage. In summary, our study suggests that PD0166285, an inhibitor of Wee1, sensitizes LUSC cells to cisplatin and modulates DNA damage and apoptosis pathways through Rad51 and Stat1, respectively. These findings highlight the combination of PD0166285 and cisplatin as a promising therapeutic approach for treating LUSC.
{"title":"Wee1 inhibitor PD0166285 sensitized TP53 mutant lung squamous cell carcinoma to cisplatin via STAT1","authors":"Qi Li, Wenjie Yang, Qingyi Zhang, Daoming Zhang, Jun Deng, Binxin Chen, Ping Li, Huanqi Zhang, Yiming Jiang, Yangling Li, Bo Zhang, Nengming Lin","doi":"10.1186/s12935-024-03489-w","DOIUrl":"https://doi.org/10.1186/s12935-024-03489-w","url":null,"abstract":"Lung squamous cell carcinoma (LUSCs) is associated with high mortality (20–30%) and lacks of effective treatments. Almost all LUSC exhibit somatic mutations in TP53. Wee1, a tyrosine kinase, regulates the cell cycle at the G2/M checkpoint. In TP53-deficient cells, the dependence on G2/M checkpoints increases. PD0166285 is the first reported drug with inhibitory activity against both Wee1 and PKMYT1. Protein expression was determined by Western blot analysis. Cell proliferation was assessed using cell colony formation and CCK-8 assays. Cell cycle was performed by PI staining with flow cytometry. Apoptosis was evaluated using Annexin V-Phycoerythrin double staining and flow cytometry. DNA damage was detected through comet assay and immunofluorescence assay. In vivo, apoptosis and anti-tumor effects were assessed using the TUNEL assay, a nude mouse model, and immunohistochemistry (IHC). Co-immunoprecipitation assay was used to detect protein–protein interactions. We analyzed Wee1, PKMYT1, and Stat1 expression in pan-cancer studies using the Ualcan public database and assessed their prognostic implications with Kaplan–Meier curves. PD0166285, a Wee1 inhibitor, effectively inhibits Wee1 activity, promoting cell entry into a mitotic crisis. Moreover, PD0166285 sensitizes cells to cisplatin, enhancing clinical outcomes. Our study demonstrated that PD016628 regulates the cell cycle through Rad51 and results in cell cycle arrest at the G2/M phase. We observed increased apoptosis in tumor cells treated with PD0166285, particularly when combined with cisplatin, indicating an enhanced apoptotic response. The upregulation of γ-H2AX serves as an indicator of mitotic catastrophe. Co-immunoprecipitation and data analysis revealed that apoptosis in LUSC is mediated through the Stat1 pathway, accompanied by decreased levels of Socs3. Furthermore, IHC staining confirmed significant differences in the expression of Phospho-CDK1 and γ-H2AX in LUSCs, suggesting involvement in DNA damage. In summary, our study suggests that PD0166285, an inhibitor of Wee1, sensitizes LUSC cells to cisplatin and modulates DNA damage and apoptosis pathways through Rad51 and Stat1, respectively. These findings highlight the combination of PD0166285 and cisplatin as a promising therapeutic approach for treating LUSC.","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"1 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142203350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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/s12935-024-03486-z
Jun Chen, Tingting Wu, Yongwen Yang
Sialylation in uterine corpus endometrial carcinoma (UCEC) differs significantly from apoptotic and ferroptosis pathways. It plays a crucial role in cancer progression and immune response modulation. Exploring how sialylation affects tumor behavior and its link with long non-coding RNAs (lncRNAs) may provide new insights into UCEC prognosis and treatment. We obtained RNA transcriptome, clinical, and mutation data of UCEC samples from the TCGA database. Our approach involved developing a risk model based on the co-expression patterns of sialylation genes and lncRNAs. Prognostic lncRNAs were identified through Cox regression and further refined using LASSO analysis. To understand the biological functions and pathways of model-associated differentially expressed genes (MADEGs), we conducted enrichment analyses. We also assessed the immune infiltration status of MADEGs using eight different algorithms, which helped in evaluating the potential for immunotherapy. Additionally, we validated the expression of these lncRNAs in UCEC using cell lines and clinical samples. We developed a UCEC risk model using five sialylation-related lncRNAs (AC004884.2, AC026202.2, LINC01579, LINC00942, SLC16A1-AS1). This model, confirmed through Cox analysis and clinical evaluation, effectively predicted patient outcomes. Survival data analysis across entire cohort, as well as within training and test groups, indicated better survival in low-risk UCEC patients. Enrichment analyses linked MADEGs to sialylation functions and cancer pathways. High-risk patients showed increased responsiveness to immune checkpoint inhibitors (ICIs), as indicated by immunological assessments. Subgroup C2 patients showed superior outcomes and a robust response to immunotherapy and chemotherapy. Notably, LINC01579, LINC00942, and SLC16A1-AS1 were significantly overexpressed in UCEC clinical tumor samples as well as in Ishikawa and HEC-1-B cell lines, compared to the normal groups. This lncRNA signature associated with sialylation could guide prognosis, enhance the understanding of molecular mechanisms, and inform treatment strategies in UCEC. It highlights the potential for the use of ICIs and chemotherapy.
{"title":"Sialylation-associated long non-coding RNA signature predicts the prognosis, tumor microenvironment, and immunotherapy and chemotherapy options in uterine corpus endometrial carcinoma","authors":"Jun Chen, Tingting Wu, Yongwen Yang","doi":"10.1186/s12935-024-03486-z","DOIUrl":"https://doi.org/10.1186/s12935-024-03486-z","url":null,"abstract":"Sialylation in uterine corpus endometrial carcinoma (UCEC) differs significantly from apoptotic and ferroptosis pathways. It plays a crucial role in cancer progression and immune response modulation. Exploring how sialylation affects tumor behavior and its link with long non-coding RNAs (lncRNAs) may provide new insights into UCEC prognosis and treatment. We obtained RNA transcriptome, clinical, and mutation data of UCEC samples from the TCGA database. Our approach involved developing a risk model based on the co-expression patterns of sialylation genes and lncRNAs. Prognostic lncRNAs were identified through Cox regression and further refined using LASSO analysis. To understand the biological functions and pathways of model-associated differentially expressed genes (MADEGs), we conducted enrichment analyses. We also assessed the immune infiltration status of MADEGs using eight different algorithms, which helped in evaluating the potential for immunotherapy. Additionally, we validated the expression of these lncRNAs in UCEC using cell lines and clinical samples. We developed a UCEC risk model using five sialylation-related lncRNAs (AC004884.2, AC026202.2, LINC01579, LINC00942, SLC16A1-AS1). This model, confirmed through Cox analysis and clinical evaluation, effectively predicted patient outcomes. Survival data analysis across entire cohort, as well as within training and test groups, indicated better survival in low-risk UCEC patients. Enrichment analyses linked MADEGs to sialylation functions and cancer pathways. High-risk patients showed increased responsiveness to immune checkpoint inhibitors (ICIs), as indicated by immunological assessments. Subgroup C2 patients showed superior outcomes and a robust response to immunotherapy and chemotherapy. Notably, LINC01579, LINC00942, and SLC16A1-AS1 were significantly overexpressed in UCEC clinical tumor samples as well as in Ishikawa and HEC-1-B cell lines, compared to the normal groups. This lncRNA signature associated with sialylation could guide prognosis, enhance the understanding of molecular mechanisms, and inform treatment strategies in UCEC. It highlights the potential for the use of ICIs and chemotherapy.","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"100 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142203351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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/s12935-024-03495-y
Jiri Navratil, Monika Kratochvilova, Martina Raudenska, Jan Balvan, Tomas Vicar, Katerina Petrlakova, Kanako Suzuki, Lucie Jadrna, Jiri Bursa, Martin Kräter, Kyoohyun Kim, Michal Masarik, Jaromir Gumulec
The failure of intracellular zinc accumulation is a key process in prostate carcinogenesis. Although prostate cancer cells can accumulate zinc after long-term exposure, chronic zinc oversupply may accelerate prostate carcinogenesis or chemoresistance. Because cancer progression is associated with energetically demanding cytoskeletal rearrangements, we investigated the effect of long-term zinc presence on biophysical parameters, ATP production, and EMT characteristics of two prostate cancer cell lines (PC-3, 22Rv1). Prolonged exposure to zinc increased ATP production, spare respiratory capacity, and induced a response in PC-3 cells, characterized by remodeling of vimentin and a shift of cell dry mass density and caveolin-1 to the perinuclear region. This zinc-induced remodeling correlated with a greater tendency to maintain actin architecture despite inhibition of actin polymerization by cytochalasin. Zinc partially restored epithelial characteristics in PC-3 cells by decreasing vimentin expression and increasing E-cadherin. Nevertheless, the expression of E-cadherin remained lower than that observed in predominantly oxidative, low-invasive 22Rv1 cells. Following long-term zinc exposure, we observed an increase in cell stiffness associated with an increased refractive index in the perinuclear region and an increased mitochondrial content. The findings of the computational simulations indicate that the mechanical response cannot be attributed exclusively to alterations in cytoskeletal composition. This observation suggests the potential involvement of an additional, as yet unidentified, mechanical contributor. These findings indicate that long-term zinc exposure alters a group of cellular parameters towards an invasive phenotype, including an increase in mitochondrial number, ATP production, and cytochalasin resistance. Ultimately, these alterations are manifested in the biomechanical properties of the cells.
{"title":"Long-term zinc treatment alters the mechanical properties and metabolism of prostate cancer cells","authors":"Jiri Navratil, Monika Kratochvilova, Martina Raudenska, Jan Balvan, Tomas Vicar, Katerina Petrlakova, Kanako Suzuki, Lucie Jadrna, Jiri Bursa, Martin Kräter, Kyoohyun Kim, Michal Masarik, Jaromir Gumulec","doi":"10.1186/s12935-024-03495-y","DOIUrl":"https://doi.org/10.1186/s12935-024-03495-y","url":null,"abstract":"The failure of intracellular zinc accumulation is a key process in prostate carcinogenesis. Although prostate cancer cells can accumulate zinc after long-term exposure, chronic zinc oversupply may accelerate prostate carcinogenesis or chemoresistance. Because cancer progression is associated with energetically demanding cytoskeletal rearrangements, we investigated the effect of long-term zinc presence on biophysical parameters, ATP production, and EMT characteristics of two prostate cancer cell lines (PC-3, 22Rv1). Prolonged exposure to zinc increased ATP production, spare respiratory capacity, and induced a response in PC-3 cells, characterized by remodeling of vimentin and a shift of cell dry mass density and caveolin-1 to the perinuclear region. This zinc-induced remodeling correlated with a greater tendency to maintain actin architecture despite inhibition of actin polymerization by cytochalasin. Zinc partially restored epithelial characteristics in PC-3 cells by decreasing vimentin expression and increasing E-cadherin. Nevertheless, the expression of E-cadherin remained lower than that observed in predominantly oxidative, low-invasive 22Rv1 cells. Following long-term zinc exposure, we observed an increase in cell stiffness associated with an increased refractive index in the perinuclear region and an increased mitochondrial content. The findings of the computational simulations indicate that the mechanical response cannot be attributed exclusively to alterations in cytoskeletal composition. This observation suggests the potential involvement of an additional, as yet unidentified, mechanical contributor. These findings indicate that long-term zinc exposure alters a group of cellular parameters towards an invasive phenotype, including an increase in mitochondrial number, ATP production, and cytochalasin resistance. Ultimately, these alterations are manifested in the biomechanical properties of the cells.","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"54 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142203384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-10DOI: 10.1186/s12935-024-03490-3
Bo Wang, Jiahui Mao, Linxia Wang, Yuexin Zhao, Bingying Wang, Huan Yang
This study aims to explore the molecular mechanism of lncRNA RP3-340B19.3 on breast cancer cell proliferation and metastasis and clinical significance of lncRNA RP3-340B19.3 for breast cancer. The subcellular localization of lncRNA RP3-340B19.3 was identified using RNA fluorescence in situ hybridization (FISH). The expression of lncRNA RP3-340B19.3 in breast cancer cells, breast cancer tissues, as well as the serum and serum exosomes of breast cancer patients, was measured through quantitative RT-PCR. In the in vitro setting, we conducted experiments to observe the effects of RP3-340B19.3 on both cell migration and proliferation. This was achieved through the utilization of transwell migration assays as well as clone formation assays. Meanwhile, transwell migration assays and clone formation assays were used to observe the effects of MDA-MB-231-exosomes enriched in RP3-340B19.3 on breast cancer microenvironment cells MCF7 and BMMSCs. Additionally, western blotting techniques were used to assess the expression levels of proteins associated with essential cellular processes such as proliferation, apoptosis, and metastasis. In vivo, the impact of RP3-340B19.3 knockdown on tumour weight and volume was observed within a nude mice model. We aimed to delve into the intricate molecular mechanisms involving RP3-340B19.3 by using bioinformatics analysis, dual luciferase reporter gene experiments and western blotting. Moreover, the potential correlations between RP3-340B19.3 expression and various clinical pathological characteristics were analyzed. Our investigation revealed that RP3-340B19.3 was expressed in both the cytoplasm and nucleus, with a noteworthy increase in breast cancer cells. Notably, we found that RP3-340B19.3 exerted a promoting influence on the proliferation and migration of breast cancer cells, both in vitro and in vivo. MDA-MB-231-exosomes enriched in RP3-340B19.3 promoted the proliferation and migration of MCF7 and BMMSCs in vitro. Mechanistically, RP3-340B19.3 demonstrated the capability to modulate the expression of MORC4 by forming a complex with miR-4510. This interaction subsequently triggered the activation of the NF-κB and Wnt-β-catenin signaling pathways. Furthermore, our study highlighted the potential diagnostic utility of RP3-340B19.3. We discovered its presence in the serum and exosomes of breast cancer patients, showing promising efficacy as a diagnostic marker. Notably, the diagnostic potential of RP3-340B19.3 was particularly significant in relation to distinguishing between different pathological types of breast cancer and correlating with tumour diameter. Our findings establish that RP3-340B19.3 plays a pivotal role in driving the proliferation and metastasis of breast cancer. Additionally, exosomes enriched in RP3-340B19.3 could influence MCF7 and BMMSCs in tumour microenvironment, promoting the progression of breast cancer. This discovery positions RP3-340B19.3 as a prospective novel candidate for a tumour marker, of
{"title":"Exosome-mediated transfer of lncRNA RP3-340B19.3 promotes the progression of breast cancer by sponging miR-4510/MORC4 axis","authors":"Bo Wang, Jiahui Mao, Linxia Wang, Yuexin Zhao, Bingying Wang, Huan Yang","doi":"10.1186/s12935-024-03490-3","DOIUrl":"https://doi.org/10.1186/s12935-024-03490-3","url":null,"abstract":"This study aims to explore the molecular mechanism of lncRNA RP3-340B19.3 on breast cancer cell proliferation and metastasis and clinical significance of lncRNA RP3-340B19.3 for breast cancer. The subcellular localization of lncRNA RP3-340B19.3 was identified using RNA fluorescence in situ hybridization (FISH). The expression of lncRNA RP3-340B19.3 in breast cancer cells, breast cancer tissues, as well as the serum and serum exosomes of breast cancer patients, was measured through quantitative RT-PCR. In the in vitro setting, we conducted experiments to observe the effects of RP3-340B19.3 on both cell migration and proliferation. This was achieved through the utilization of transwell migration assays as well as clone formation assays. Meanwhile, transwell migration assays and clone formation assays were used to observe the effects of MDA-MB-231-exosomes enriched in RP3-340B19.3 on breast cancer microenvironment cells MCF7 and BMMSCs. Additionally, western blotting techniques were used to assess the expression levels of proteins associated with essential cellular processes such as proliferation, apoptosis, and metastasis. In vivo, the impact of RP3-340B19.3 knockdown on tumour weight and volume was observed within a nude mice model. We aimed to delve into the intricate molecular mechanisms involving RP3-340B19.3 by using bioinformatics analysis, dual luciferase reporter gene experiments and western blotting. Moreover, the potential correlations between RP3-340B19.3 expression and various clinical pathological characteristics were analyzed. Our investigation revealed that RP3-340B19.3 was expressed in both the cytoplasm and nucleus, with a noteworthy increase in breast cancer cells. Notably, we found that RP3-340B19.3 exerted a promoting influence on the proliferation and migration of breast cancer cells, both in vitro and in vivo. MDA-MB-231-exosomes enriched in RP3-340B19.3 promoted the proliferation and migration of MCF7 and BMMSCs in vitro. Mechanistically, RP3-340B19.3 demonstrated the capability to modulate the expression of MORC4 by forming a complex with miR-4510. This interaction subsequently triggered the activation of the NF-κB and Wnt-β-catenin signaling pathways. Furthermore, our study highlighted the potential diagnostic utility of RP3-340B19.3. We discovered its presence in the serum and exosomes of breast cancer patients, showing promising efficacy as a diagnostic marker. Notably, the diagnostic potential of RP3-340B19.3 was particularly significant in relation to distinguishing between different pathological types of breast cancer and correlating with tumour diameter. Our findings establish that RP3-340B19.3 plays a pivotal role in driving the proliferation and metastasis of breast cancer. Additionally, exosomes enriched in RP3-340B19.3 could influence MCF7 and BMMSCs in tumour microenvironment, promoting the progression of breast cancer. This discovery positions RP3-340B19.3 as a prospective novel candidate for a tumour marker, of","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"8 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142203354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Currently, there are no optimal biomarkers available for distinguishing patients who will respond to immune checkpoint inhibitors (ICIs) therapies. Consequently, the exploration of novel biomarkers that can predict responsiveness to ICIs is crucial in the field of immunotherapy. We estimated the proportions of 22 immune cell components in 10 cancer types (6,128 tumors) using the CIBERSORT algorithm, and further classified patients based on their tumor immune cell proportions in a pan-cancer setting using k-means clustering. Differentially expressed immune genes between the patient subgroups were identified, and potential predictive biomarkers for ICIs were explored. Finally, the predictive value of the identified biomarkers was verified in patients with urothelial carcinoma (UC) and esophageal squamous cell carcinoma (ESCC) who received ICIs. Our study identified two subgroups of patients with distinct immune infiltrating phenotypes and differing clinical outcomes. The patient subgroup with improved outcomes displayed tumors enriched with genes related to immune response regulation and pathway activation. Furthermore, CCL5 and CSF2 were identified as immune-related hub-genes and were found to be prognostic in a pan-cancer setting. Importantly, UC and ESCC patients with high expression of CCL5 and low expression of CSF2 responded better to ICIs. We demonstrated CCL5 and CSF2 as potential novel biomarkers for predicting the response to ICIs in patients with UC and ESCC. The predictive value of these biomarkers in other cancer types warrants further evaluation in future studies.
{"title":"Pan-cancer analysis reveals CCL5/CSF2 as potential predictive biomarkers for immune checkpoint inhibitors","authors":"Yi-Chao Chen, Wei-Zhong Zheng, Chun-Peng Liu, Yong-Qiang Zhao, Jun-Wei Li, Ze-Sen Du, Tian-Tian Zhai, Hao-Yu Lin, Wen-Qi Shi, Shan-Qing Cai, Feng Pan, Si-Qi Qiu","doi":"10.1186/s12935-024-03496-x","DOIUrl":"https://doi.org/10.1186/s12935-024-03496-x","url":null,"abstract":"Currently, there are no optimal biomarkers available for distinguishing patients who will respond to immune checkpoint inhibitors (ICIs) therapies. Consequently, the exploration of novel biomarkers that can predict responsiveness to ICIs is crucial in the field of immunotherapy. We estimated the proportions of 22 immune cell components in 10 cancer types (6,128 tumors) using the CIBERSORT algorithm, and further classified patients based on their tumor immune cell proportions in a pan-cancer setting using k-means clustering. Differentially expressed immune genes between the patient subgroups were identified, and potential predictive biomarkers for ICIs were explored. Finally, the predictive value of the identified biomarkers was verified in patients with urothelial carcinoma (UC) and esophageal squamous cell carcinoma (ESCC) who received ICIs. Our study identified two subgroups of patients with distinct immune infiltrating phenotypes and differing clinical outcomes. The patient subgroup with improved outcomes displayed tumors enriched with genes related to immune response regulation and pathway activation. Furthermore, CCL5 and CSF2 were identified as immune-related hub-genes and were found to be prognostic in a pan-cancer setting. Importantly, UC and ESCC patients with high expression of CCL5 and low expression of CSF2 responded better to ICIs. We demonstrated CCL5 and CSF2 as potential novel biomarkers for predicting the response to ICIs in patients with UC and ESCC. The predictive value of these biomarkers in other cancer types warrants further evaluation in future studies.","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"5 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142203352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Colon adenocarcinoma (COAD) represents a significant health concern within the population. Advancing our understanding of COAD is imperative for early detection, enabling personalized treatment interventions, and facilitating the development of effective preventive measures. The coagulation system plays a role in tumor-related pathological processes; however, its specific involvement in COAD and potential contributors remain unclear. This study aimed to establish a novel risk stratification approach by analyzing coagulation related genes (CRGs) associated with COAD. Through a comprehensive bioinformatics analysis of data from public databases, we screened COAD associated CRGs and characterized the associated molecular subtypes. After a comprehensive analysis of the characteristics of each subtype, we applied differentially expressed genes in CRG subtypes to establish a new risk stratification method. Clinical subgroup analysis, immunoinfiltration analysis, therapeutic reactivity prediction and other analytical methods suggest the potential clinical value of the established risk stratification method. As one of the selected targets, the effect of MS4A4A on the proliferation and invasion of COAD was confirmed by in vitro experiments, which partially verified the reliability of bioinformatics results. Our findings delineate CRGs potentially implicated in COAD pathogenesis and offer fresh insights into the influence of the coagulation process on tumorigenesis and progression.
{"title":"A novel risk stratification approach and molecular subgroup characterization based on coagulation related genes in colon adenocarcinoma","authors":"Xiangxin Wu, Lichong Zhu, Xizhe Sun, Mingyu Xia, Shihui Zhao, Bomiao Zhang, Tianyi Xia","doi":"10.1186/s12935-024-03491-2","DOIUrl":"https://doi.org/10.1186/s12935-024-03491-2","url":null,"abstract":"Colon adenocarcinoma (COAD) represents a significant health concern within the population. Advancing our understanding of COAD is imperative for early detection, enabling personalized treatment interventions, and facilitating the development of effective preventive measures. The coagulation system plays a role in tumor-related pathological processes; however, its specific involvement in COAD and potential contributors remain unclear. This study aimed to establish a novel risk stratification approach by analyzing coagulation related genes (CRGs) associated with COAD. Through a comprehensive bioinformatics analysis of data from public databases, we screened COAD associated CRGs and characterized the associated molecular subtypes. After a comprehensive analysis of the characteristics of each subtype, we applied differentially expressed genes in CRG subtypes to establish a new risk stratification method. Clinical subgroup analysis, immunoinfiltration analysis, therapeutic reactivity prediction and other analytical methods suggest the potential clinical value of the established risk stratification method. As one of the selected targets, the effect of MS4A4A on the proliferation and invasion of COAD was confirmed by in vitro experiments, which partially verified the reliability of bioinformatics results. Our findings delineate CRGs potentially implicated in COAD pathogenesis and offer fresh insights into the influence of the coagulation process on tumorigenesis and progression.","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"59 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142203385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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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