Oncogene最新文献_第6页

Slc7a5 promotes T cell anti-tumor immunity through sustaining cytotoxic T lymphocyte effector function Slc7a5通过维持细胞毒性T淋巴细胞效应功能促进T细胞抗肿瘤免疫。

IF 7.3 1区医学

Oncogene Pub Date : 2025-08-26 DOI: 10.1038/s41388-025-03543-5

Chunwan Lu, Liyan Liang, Yanmin Wu, Yingcui Yang, Dakota Poschel, Yang Zhao, Lirong Pei, Miao Yu, Martina Zoccheddu, Sergei Bombin, Han-Fei Ding, Huidong Shi, Kebin Liu

{"title":"Slc7a5 promotes T cell anti-tumor immunity through sustaining cytotoxic T lymphocyte effector function","authors":"Chunwan Lu, Liyan Liang, Yanmin Wu, Yingcui Yang, Dakota Poschel, Yang Zhao, Lirong Pei, Miao Yu, Martina Zoccheddu, Sergei Bombin, Han-Fei Ding, Huidong Shi, Kebin Liu","doi":"10.1038/s41388-025-03543-5","DOIUrl":"10.1038/s41388-025-03543-5","url":null,"abstract":"Tryptophan (Trp) metabolites have emerged as key regulators of host tumor immunity and cancer patient response to immunotherapy. However, the function of and mechanism underlying Trp in tumor-activated CTLs in the tumor microenvironment are incompletely understood. Using a defined co-culture system of tumor-specific CTLs and cognate antigen-expressing tumor cells, we performed a genome-wide metabolomics screening and observed that Trp level is elevated in the tumor cell-activated CTLs. Parallel genome-wide RNA-Sequencing and ATAC-Sequencing analysis determined that tumor-specific CTLs respond to tumor cells by transcriptionally activating Slc7a5 expression. Pharmacological inhibition of Slc7a5 decreased Trp uptake in tumor-activated CTLs and suppressed CTL lytic activity in killing tumor cells in vitro. Mice with Slc7a5 deficiency only in T cells exhibited diminished level of tumor-infiltrating T cells and increased tumor growth and metastasis. scRNA-sequencing analysis revealed that Slc7a5 deficiency resulted in decreased activation of the aryl hydrocarbon receptor (AhR) pathway and repressed FasL expression in tumor-infiltrating T cells. Chromatin immunoprecipitation determined that AhR binds to Faslg promoter in tumor-infiltrating T cells. FasL blockade therapy promotes tumor growth and metastasis in tumor-bearing mice. In human cancer patients, AhR expression correlates with FasL expression in tumor-infiltrating T cells. Furthermore, FasL expression is correlated with patient response to pembrolizumab and survival time. Our finding determines that the Slc7a5-Trp metabolic pathway activates AhR to up-regulate FasL expression in tumor-infiltrating T cells to sustain CTL anti-tumor immunity. Targeting CAR-T cells to up-regulate Slc7a5 to maintain T cell proliferation and function therefore could be a promising direction in cancer immunotherapy.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"44 41","pages":"3939-3954"},"PeriodicalIF":7.3,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963702","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}

引用次数: 0

GABAergic signaling contributes to tumor cell invasion and poor overall survival in colorectal cancer gaba能信号导致结直肠癌的肿瘤细胞侵袭和较差的总生存率。

IF 7.3 1区医学

Oncogene Pub Date : 2025-08-24 DOI: 10.1038/s41388-025-03546-2

Carly Strelez, Francesca Battaglin, Rachel Perez, Yan Yang, Christopher Cherry, Joshua Millstein, Ah Young Yoon, John S. Chlystek, Ethan Canfield, Bethany Haliday, Curran Shah, Kimya Ghaffarian, Shivani Soni, Hannah Jiang, Roy Lau, Aaron Schatz, Yuyuan Zhou, Daniel Mulkerin, Fang-Shu Ou, Alan P. Venook, Federico Innocenti, Josh Neman, Jonathan E. Katz, Heinz-Josef Lenz, Shannon M. Mumenthaler

{"title":"GABAergic signaling contributes to tumor cell invasion and poor overall survival in colorectal cancer","authors":"Carly Strelez, Francesca Battaglin, Rachel Perez, Yan Yang, Christopher Cherry, Joshua Millstein, Ah Young Yoon, John S. Chlystek, Ethan Canfield, Bethany Haliday, Curran Shah, Kimya Ghaffarian, Shivani Soni, Hannah Jiang, Roy Lau, Aaron Schatz, Yuyuan Zhou, Daniel Mulkerin, Fang-Shu Ou, Alan P. Venook, Federico Innocenti, Josh Neman, Jonathan E. Katz, Heinz-Josef Lenz, Shannon M. Mumenthaler","doi":"10.1038/s41388-025-03546-2","DOIUrl":"10.1038/s41388-025-03546-2","url":null,"abstract":"Alterations in neurotransmitter signaling can influence colorectal cancer (CRC). In a large, randomized Phase III clinical trial (CALGB/SWOG 80405) involving patients with metastatic CRC, high expression of gamma-aminobutyric acid (GABA) pathway gene GAD1 and low expression of ABAT, indicative of a GABAergic environment, were associated with worse progression-free survival and overall survival outcomes. A metastasis map of human cancer cell lines (MetMap) and functional studies using a microfluidic tumor-on-chip platform demonstrated that high GAD1 expression correlates with increased metastatic potential. Knockdown and pharmacological inhibition of GAD1 reduced tumor invasion, while exogenous GABA promoted invasion. Tumor-derived GABA was elevated in Ras-altered tumors. Furthermore, analysis of publicly available data confirmed that higher GAD1 expression is associated with worse outcomes in Ras-mutant tumors. These findings establish a role for GABA signaling in tumor invasiveness, particularly in Ras-altered CRC. This study demonstrates using clinical data to inform new discoveries and highlights the need for advanced preclinical model systems that more accurately reflect human physiology to explore these findings.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"44 41","pages":"3924-3938"},"PeriodicalIF":7.3,"publicationDate":"2025-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41388-025-03546-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RCN3 functions as a tumor promoter in colorectal cancer by modulating the GRP78-PI3K-AKT signaling pathway RCN3通过调节GRP78-PI3K-AKT信号通路在结直肠癌中发挥肿瘤启动子的作用。

IF 7.3 1区医学

Oncogene Pub Date : 2025-08-23 DOI: 10.1038/s41388-025-03535-5

Mei Huang, Bingru Qin, Zhefan Xie, Ruling Zhou, Zhizhao Lin, Lihua Zhou, Zelong Han, Side Liu, Kangmin Zhuang

{"title":"RCN3 functions as a tumor promoter in colorectal cancer by modulating the GRP78-PI3K-AKT signaling pathway","authors":"Mei Huang, Bingru Qin, Zhefan Xie, Ruling Zhou, Zhizhao Lin, Lihua Zhou, Zelong Han, Side Liu, Kangmin Zhuang","doi":"10.1038/s41388-025-03535-5","DOIUrl":"10.1038/s41388-025-03535-5","url":null,"abstract":"Colorectal cancer (CRC) remains a significant global health concern, highlighting the urgent need for novel therapeutic targets and prognostic biomarkers. This study investigates the role of Reticulocalbin-3 (RCN3) in CRC development, focusing on its regulatory influence on calcium ion homeostasis and transport proteins, critical factors in cancer progression. We employed bioinformatics databases, qRT-PCR, Western blotting, and immunohistochemistry to evaluate RCN3 expression levels, revealing that RCN3 is upregulated in CRC tissues and correlates with poorer patient outcomes. Functional assays demonstrated that alterations in RCN3 expression significantly accelerated cell proliferation, migration, and invasion of CRC cells both in vitro and in vivo. Mechanistically, the interaction of RCN3’s EF-hand domains 3 and 4 with glucose-regulated protein 78 (GRP78) promotes its translocation to the cellular membrane, inducing endoplasmic reticulum stress through elevated intracellular calcium levels. Furthermore, RCN3 was found to regulate the PI3K-AKT-mTOR-S6 signaling pathway by enhancing the phosphorylation of key proteins, thereby emphasizing its multifaceted role in CRC pathogenesis. In conclusion, these findings suggest that RCN3 not only contributes to CRC progression but also holds promise as a potential therapeutic target and biomarker for improving patient outcomes in CRC management.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"44 40","pages":"3850-3863"},"PeriodicalIF":7.3,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963663","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}

引用次数: 0

HOMER3 orchestrates SRC-YAP1 activity that promotes tumor cell growth and antagonizes anti-tumor immunotherapy in prostate cancer 在前列腺癌中，HOMER3协调SRC-YAP1活性，促进肿瘤细胞生长并拮抗抗肿瘤免疫治疗。

IF 7.3 1区医学

Oncogene Pub Date : 2025-08-23 DOI: 10.1038/s41388-025-03548-0

Tongyu Tong, Hanqi Lei, Mengjun Huang, Zheng Yang, Xuyin Dai, Hailin Zou, Yibo Guo, Juan Luo, Qiliang Teng, Fei Cao, Jun Pang, Peng Li

{"title":"HOMER3 orchestrates SRC-YAP1 activity that promotes tumor cell growth and antagonizes anti-tumor immunotherapy in prostate cancer","authors":"Tongyu Tong, Hanqi Lei, Mengjun Huang, Zheng Yang, Xuyin Dai, Hailin Zou, Yibo Guo, Juan Luo, Qiliang Teng, Fei Cao, Jun Pang, Peng Li","doi":"10.1038/s41388-025-03548-0","DOIUrl":"10.1038/s41388-025-03548-0","url":null,"abstract":"(Yes-associated protein 1) YAP1 is frequently activated in human prostate cancers (PCa), but the underlying regulatory mechanism remains elusive. Here, we identified a novel scaffold protein HOMER3 in PCa, that can promote YAP1 activity by disrupting LATS-YAP1 phosphorylation. Mechanistically, HOMER3 overexpression in PCa facilitates the SRC kinase to phosphorylate YAP1 accompanied by counteracting LATS1-mediated YAP1 inhibition, thereby maintaining high YAP1 nuclear localization and transcriptional activity. Accordingly, HOMER3 gain-of-function in PCa cells phenocopies the effect of YAP1 activation, including cell hyperproliferation in vitro and rapid tumor growth in vivo. Additionally, transcriptome analysis revealed that CD274 is consistently upregulated in HOMER3 overexpressing PCa cells and patients, which eventually contributed to an immunosuppressive phenotype. More importantly, blocking SRC kinase-mediated YAP1 activation improved the immunotherapy-insensitive phenotypes in PCa caused by HOMER3 overexpression. Taken together, our findings define a novel kinase-substrate interactive platform for HOMER3 to orchestrate YAP1 activity in PCa. Targeting SRC-YAP1 oncogenic axis provides new insights into the therapeutic potential for PCa patients carried HOMER3 overexpression.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"44 41","pages":"3895-3908"},"PeriodicalIF":7.3,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963567","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}

引用次数: 0

LGI3 promotes the progression of TFE3-rearranged renal cell carcinoma through GEMIN6/AURKB axis LGI3通过GEMIN6/AURKB轴促进tfe3重排肾细胞癌的进展。

IF 7.3 1区医学

Oncogene Pub Date : 2025-08-23 DOI: 10.1038/s41388-025-03553-3

Junxiao Liu, Huayi Feng, Zhuang Xiong, Shouqing Cao, Tianwei Cai, Wenjie Wei, Wen Tao, Xu Zhang, Xin Ma, Xiubin Li

{"title":"LGI3 promotes the progression of TFE3-rearranged renal cell carcinoma through GEMIN6/AURKB axis","authors":"Junxiao Liu, Huayi Feng, Zhuang Xiong, Shouqing Cao, Tianwei Cai, Wenjie Wei, Wen Tao, Xu Zhang, Xin Ma, Xiubin Li","doi":"10.1038/s41388-025-03553-3","DOIUrl":"10.1038/s41388-025-03553-3","url":null,"abstract":"Transcription factor binding to IGHM enhancer 3-rearranged renal cell carcinoma (TFE3-RCC) is characterized by its aggressive nature, limited treatment options, and poor prognosis. However, the downstream targets of TFE3 fusion protein responsible for its tumorigenesis and progression remain unclear. Here, we demonstrated that leucine-rich repeat LGI family member 3 (LGI3) is a direct target of TFE3 fusion protein. TFE3 fusion protein can bind to the promoter of LGI3 and then activate its transcription. Importantly, LGI3 contributes to the proliferation, migration, and invasion of TFE3-RCC. Mechanistically, LGI3 interacts with gem nuclear organelle-associated protein 6 (GEMIN6) and inhibits its degradation via decreasing its ubiquitination. GEMIN6 upregulation promotes the mRNA maturation of Aurora B kinase (AURKB), thereby promoting the progression of TFE3-RCC. Importantly, drugs targeting GEMIN6 or AURKB significantly suppressed the growth of TFE3-RCC cells and organoids. In human TFE3-RCC tissues, LGI3 is highly expressed and positively correlated with GEMIN6 and AURKB. Overall, we revealed a novel mechanism underlying the progression of TFE3-RCC and provided potential new therapeutic targets.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"44 39","pages":"3729-3740"},"PeriodicalIF":7.3,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963681","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}

引用次数: 0

Molecular and epigenetic oncogenesis in synovial sarcoma: implications for cancer biology, diagnosis and treatment 滑膜肉瘤的分子和表观遗传肿瘤发生：对癌症生物学、诊断和治疗的意义。

IF 7.3 1区医学

Oncogene Pub Date : 2025-08-23 DOI: 10.1038/s41388-025-03547-1

Amy Xueqi Wang, Kevin B. Jones, Torsten O. Nielsen

引用次数: 0

Leveraging RAS-mSIN1 interaction to selectively inhibit mTORC2 employing competitive RAS binding peptide: implications in breast cancer metastasis 利用RAS- msin1相互作用，利用竞争性RAS结合肽选择性抑制mTORC2：在乳腺癌转移中的意义

IF 7.3 1区医学

Oncogene Pub Date : 2025-08-23 DOI: 10.1038/s41388-025-03516-8

Javed Miyan, Narayan Kumar, Moinuddin, Showkat Ahmad Malik, Usmani Mohammed Akif, Rohil Hameed, Riyazuddin Mohammed, Parul Dubey, Jhajan lal, Akhilesh Kumar, Harshita Dubkara, Karthik Ramalingam, Deepali Pandey, Jiaur Rahaman Gayen, Sanjeev Kanojiya, Aamir Nazir, Wahajul Haq, Damodara N. Reddy, Ashish Arora, Ravishankar Ramachandran, Smrati Bhadauria

{"title":"Leveraging RAS-mSIN1 interaction to selectively inhibit mTORC2 employing competitive RAS binding peptide: implications in breast cancer metastasis","authors":"Javed Miyan, Narayan Kumar,  Moinuddin, Showkat Ahmad Malik, Usmani Mohammed Akif, Rohil Hameed, Riyazuddin Mohammed, Parul Dubey, Jhajan lal, Akhilesh Kumar, Harshita Dubkara, Karthik Ramalingam, Deepali Pandey, Jiaur Rahaman Gayen, Sanjeev Kanojiya, Aamir Nazir, Wahajul Haq, Damodara N. Reddy, Ashish Arora, Ravishankar Ramachandran, Smrati Bhadauria","doi":"10.1038/s41388-025-03516-8","DOIUrl":"10.1038/s41388-025-03516-8","url":null,"abstract":"The pivotal role of mTORC2 in cancer progression and metastasis underscores its potential as drug target. Despite this, selective inhibition of mTORC2 without affecting mTORC1 represents an unmet need in cancer therapy. We aimed to exploit RAS-mSIN1 interaction for selective mTORC2 targeting. We developed an 11-mer peptide (S-016-1034) from the RAS-Binding-Domain of mSIN1. Cell-free Biolayer-Interferometry (BLI) studies, confirmed direct binding of S-016-1034 to Ras, unlike its scrambled counterpart. Confocal microscopy and flow-cytometry studies illustrated peptide’s cell-membrane penetration, through non-endosomal route, Cell-based assays, including immunoprecipitation and in-situ proximity-ligation, illustrated disruption of Ras-mSin1 interaction, achieving selective inhibition of mTORC2 over mTORC1. The specificity of mTORC2 inhibition was further substantiated through transcriptomics, cell-based, small model (C. elegans), and 4T1/Balb/c mouse models of breast cancer. These studies highlight the potential of Ras-binding peptide S-016-1034 in selectively inhibiting mTORC2, whereby further optimization may offer promising strategies to halt cancer cell invasion and metastasis.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"44 41","pages":"3909-3923"},"PeriodicalIF":7.3,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963647","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}

引用次数: 0

KDM1A-driven RNF81 downregulation promotes gastric cancer progression via KLF4 destabilization kdm1a驱动的RNF81下调通过KLF4不稳定促进胃癌进展。

IF 7.3 1区医学

Oncogene Pub Date : 2025-08-23 DOI: 10.1038/s41388-025-03549-z

Feng Wang, Po Hao, Yongli Pu, Xiao He, Qing He, Hongjuan Cui, Suting Jiang

{"title":"KDM1A-driven RNF81 downregulation promotes gastric cancer progression via KLF4 destabilization","authors":"Feng Wang, Po Hao, Yongli Pu, Xiao He, Qing He, Hongjuan Cui, Suting Jiang","doi":"10.1038/s41388-025-03549-z","DOIUrl":"10.1038/s41388-025-03549-z","url":null,"abstract":"Gastric cancer (GC) is a leading cause of cancer-related deaths worldwide, especially in East Asia, with a low 5-year survival rate due to late-stage diagnosis. Identifying molecular mechanisms that regulate GC progression is critical for improving clinical outcomes. RNF81, a member of the tripartite motif (TRIM) family, has demonstrated diverse roles in various cancers. In this study, we uncover its tumor-suppressive function in GC through novel regulatory pathways. Analysis of clinical data and tissue microarrays revealed that RNF81 expression is significantly downregulated in GC tissues and positively correlates with patient survival. Mechanistically, we identified lysine demethylase KDM1A as a key repressor of RNF81 expression. KDM1A recruits transcription factor E2F1 to form a transcriptional repressor complex, reducing H3K4me1 and H3K4me2 levels at the RNF81 promoter. Functional studies showed that RNF81 stabilizes the tumor suppressor KLF4 by binding through its SPRY domain, thereby inhibiting KLF4 ubiquitination and degradation. Overexpression of RNF81 suppressed GC cell proliferation, migration, and invasion in vitro and reduced tumor growth in vivo, effects that were partially rescued by KLF4 knockdown. These findings reveal a novel KDM1A-RNF81-KLF4 regulatory axis in GC and highlight RNF81 as a potential therapeutic target for GC treatment. Targeting this pathway may offer promising strategies to improve outcomes for GC patients.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"44 40","pages":"3864-3878"},"PeriodicalIF":7.3,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963675","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}

引用次数: 0

Oncogenic effects of ECM remodeling in obesity and breast cancer ECM重塑在肥胖和乳腺癌中的致癌作用。

IF 7.3 1区医学

Oncogene Pub Date : 2025-08-22 DOI: 10.1038/s41388-025-03521-x

Mackenzie L. Hawes, Marcus A. Moody, Caroline R. McCauley, Abigail G. Huddleston, Maansi Solanky, Dara H. Khosravi, Ayushi R. Patel, Ronald M. Lynch, Suresh K. Alahari, Bruce A. Bunnell, Jorge A. Belgodere, Van T. Hoang, Matthew E. Burow, Elizabeth C. Martin

{"title":"Oncogenic effects of ECM remodeling in obesity and breast cancer","authors":"Mackenzie L. Hawes, Marcus A. Moody, Caroline R. McCauley, Abigail G. Huddleston, Maansi Solanky, Dara H. Khosravi, Ayushi R. Patel, Ronald M. Lynch, Suresh K. Alahari, Bruce A. Bunnell, Jorge A. Belgodere, Van T. Hoang, Matthew E. Burow, Elizabeth C. Martin","doi":"10.1038/s41388-025-03521-x","DOIUrl":"10.1038/s41388-025-03521-x","url":null,"abstract":"Extracellular matrix (ECM) components are key regulators in breast cancer progression, as ECM remodeling is essential for breast cancer cells to invade into surrounding tissue. This process is characterized by the alignment of fibrillar collagens, breakdown of basement membrane components, and increased interstitial collagen stiffness. In patients with obesity, pre-existing ECM changes, including excessive collagen deposition and heightened matrix stiffness, mimic alterations detected in breast cancer. Given that obesity is a predictor of poor prognosis and resistance to treatment in breast cancer, it is crucial to understand how ECM conditioned by obesity affects disease outcomes. In this review, we highlight known ECM changes that occur with breast cancer and obesity and describe how these changes impact cancer cell metastasis, disease progression, and the breast cancer tumor microenvironment. We examine how obesity driven ECM remodeling affects treatment response and resistance. Further, we discuss how the compounding factor of age contributes to remodeling and current preclinical models of ECM in breast cancer.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"44 37","pages":"3409-3421"},"PeriodicalIF":7.3,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41388-025-03521-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Editorial Expression of Concern: ATM is a target for positive regulation by E2F-1 编辑表达关注：ATM是E2F-1积极监管的目标。

IF 7.3 1区医学

Oncogene Pub Date : 2025-08-19 DOI: 10.1038/s41388-025-03551-5

Eli Berkovich, Doron Ginsberg

引用次数: 0