Cell Death & Disease最新文献_第2页

Mitochondrial, metabolic and bioenergetic adaptations drive plasticity of colorectal cancer cells and shape their chemosensitivity.

IF 8.1 1区生物学

Cell Death & Disease Pub Date : 2025-04-05 DOI: 10.1038/s41419-025-07596-y

Nikita Markov, Sirina Sabirova, Gulnaz Sharapova, Marina Gomzikova, Anna Brichkina, Nick A Barlev, Marcel Egger, Albert Rizvanov, Hans-Uwe Simon

{"title":"Mitochondrial, metabolic and bioenergetic adaptations drive plasticity of colorectal cancer cells and shape their chemosensitivity.","authors":"Nikita Markov, Sirina Sabirova, Gulnaz Sharapova, Marina Gomzikova, Anna Brichkina, Nick A Barlev, Marcel Egger, Albert Rizvanov, Hans-Uwe Simon","doi":"10.1038/s41419-025-07596-y","DOIUrl":"10.1038/s41419-025-07596-y","url":null,"abstract":"The extent of mitochondrial heterogeneity and the presence of mitochondrial archetypes in cancer remain unknown. Mitochondria play a central role in the metabolic reprogramming that occurs in cancer cells. This process adjusts the activity of metabolic pathways to support growth, proliferation, and survival of cancer cells. Using a panel of colorectal cancer (CRC) cell lines, we revealed extensive differences in their mitochondrial composition, suggesting functional specialisation of these organelles. We differentiated bioenergetic and mitochondrial phenotypes, which point to different strategies used by CRC cells to maintain their sustainability. Moreover, the efficacy of various treatments targeting metabolic pathways was dependent on the respiration and glycolysis levels of cancer cells. Furthermore, we identified metabolites associated with both bioenergetic profiles and cell responses to treatments. The levels of these molecules can be used to predict the therapeutic efficacy of anti-cancer drugs and identify metabolic vulnerabilities of CRC. Our study indicates that the efficacy of CRC therapies is closely linked to mitochondrial status and cellular bioenergetics.","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"253"},"PeriodicalIF":8.1,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11971274/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Inhibition of mitochondrial complex I induces mitochondrial ferroptosis by regulating CoQH2 levels in cancer.

IF 8.1 1区生物学

Cell Death & Disease Pub Date : 2025-04-05 DOI: 10.1038/s41419-025-07510-6

Ru Deng, Lingyi Fu, Haoyu Liang, Xixiong Ai, Fangyi Liu, Nai Li, Liyan Wu, Shuo Li, Xia Yang, Yansong Lin, Yuhua Huang, Jingping Yun

{"title":"Inhibition of mitochondrial complex I induces mitochondrial ferroptosis by regulating CoQH2 levels in cancer.","authors":"Ru Deng, Lingyi Fu, Haoyu Liang, Xixiong Ai, Fangyi Liu, Nai Li, Liyan Wu, Shuo Li, Xia Yang, Yansong Lin, Yuhua Huang, Jingping Yun","doi":"10.1038/s41419-025-07510-6","DOIUrl":"10.1038/s41419-025-07510-6","url":null,"abstract":"Ferroptosis, a novel form of regulated cell death induced by the excessive accumulation of lipid peroxidation products, plays a pivotal role in the suppression of tumorigenesis. Two prominent mitochondrial ferroptosis defense systems are glutathione peroxidase 4 (GPX4) and dihydroorotate dehydrogenase (DHODH), both of which are localized within the mitochondria. However, the existence of supplementary cellular defense mechanisms against mitochondrial ferroptosis remains unclear. Our findings unequivocally demonstrate that inactivation of mitochondrial respiratory chain complex I (MCI) induces lipid peroxidation and consequently invokes ferroptosis across GPX4 low-expression cancer cells. However, in GPX4 high expression cancer cells, the MCI inhibitor did not induce ferroptosis, but increased cell sensitivity to ferroptosis induced by the GPX4 inhibitor. Overexpression of the MCI alternative protein yeast NADH-ubiquinone reductase (NDI1) not only quells ferroptosis induced by MCI inhibitors but also confers cellular protection against ferroptosis inducers. Mechanically, MCI inhibitors actuate an elevation in the NADH level while concomitantly diminishing the CoQH2 level. The manifestation of MCI inhibitor-induced ferroptosis can be reversed by supplementation with mitochondrial-specific analogues of CoQH2. Notably, MCI operates in parallel with mitochondrial-localized GPX4 and DHODH to inhibit mitochondrial ferroptosis, but independently of cytosolically localized GPX4 or ferroptosis suppressor protein 1(FSP1). The MCI inhibitor IACS-010759, is endowed with the ability to induce ferroptosis while concurrently impeding tumor proliferation in vivo. Our results identified a ferroptosis defense mechanism mediated by MCI within the mitochondria and suggested a therapeutic strategy for targeting ferroptosis in cancer treatment.","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"254"},"PeriodicalIF":8.1,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11971431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Trifluridine/tipiracil induces ferroptosis by targeting p53 via the p53-SLC7A11 axis in colorectal cancer 3D organoids.

IF 8.1 1区生物学

Cell Death & Disease Pub Date : 2025-04-05 DOI: 10.1038/s41419-025-07541-z

Maosen Huang, Yancen Wu, Xiaoxia Wei, Linyao Cheng, Lihua Fu, Haochao Yan, Wene Wei, Bo Li, Haiming Ru, Xianwei Mo, Weizhong Tang, Zijie Su, Linhai Yan

{"title":"Trifluridine/tipiracil induces ferroptosis by targeting p53 via the p53-SLC7A11 axis in colorectal cancer 3D organoids.","authors":"Maosen Huang, Yancen Wu, Xiaoxia Wei, Linyao Cheng, Lihua Fu, Haochao Yan, Wene Wei, Bo Li, Haiming Ru, Xianwei Mo, Weizhong Tang, Zijie Su, Linhai Yan","doi":"10.1038/s41419-025-07541-z","DOIUrl":"10.1038/s41419-025-07541-z","url":null,"abstract":"Trifluridine/Tipiracil (FTD/TPI, TAS102) has been approved for the treatment of patients with colorectal cancer (CRC) for its promising anticancer activity enabled by its incorporation into double strands during DNA synthesis. However, the mechanisms underlying the anticancer targets of FTD/TPI remain not fully understood. Here we report our observation of the activation of ferroptosis in CRC by FTD/TPI. Mechanistically, FTD/TPI directly promotes the ubiquitination and degradation of MDM2, thereby stabilizing the p53. Nuclear accumulation of p53 subsequently downregulates SLC7A11 expression, leading to ferroptosis. Furthermore, we observed that FTD/TPI combined with sulfasalazine (SAS), a system Xc- inhibitor, works in a synergistic manner to induce ferroptosis and further inhibit the proliferation of CRC cells. Finally, we confirmed the synergistic effect of SAS and FTD/TPI on patient-derived organoids in vitro and patient-derived xenograft mouse models in vivo. Our findings are the first to reveal that FTD/TPI induces ferroptosis via the p53-SLC7A11 axis and that SAS enhances the sensitivity and therapeutic effect of FTD/TPI. These findings suggest that the synergistic effect of FTD/TPI and SAS may represent a new therapeutic strategy for patients with CRC.","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"255"},"PeriodicalIF":8.1,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11972347/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A small molecule directly targets NLRP3 to promote inflammasome activation and antitumor immunity.

IF 8.1 1区生物学

Cell Death & Disease Pub Date : 2025-04-04 DOI: 10.1038/s41419-025-07578-0

Xuemei Liu, Hongbin He, Minghui Qi, Zhongjun Jiang, Bolong Lin, Xiaqiong Wang, Di Wang, Ming Ma, Wei Jiang, Rongbin Zhou

引用次数: 0

Cancer-associated fibroblasts secrete CSF3 to promote TNBC progression via enhancing PGM2L1-dependent glycolysis reprogramming.

IF 8.1 1区生物学

Cell Death & Disease Pub Date : 2025-04-04 DOI: 10.1038/s41419-025-07580-6

Wenqi Qin, Bing Chen, Xin Li, Wenjing Zhao, Lijuan Wang, Ning Zhang, Xiaolong Wang, Dan Luo, Yiran Liang, Yaming Li, Xi Chen, Tong Chen, Qifeng Yang

{"title":"Cancer-associated fibroblasts secrete CSF3 to promote TNBC progression via enhancing PGM2L1-dependent glycolysis reprogramming.","authors":"Wenqi Qin, Bing Chen, Xin Li, Wenjing Zhao, Lijuan Wang, Ning Zhang, Xiaolong Wang, Dan Luo, Yiran Liang, Yaming Li, Xi Chen, Tong Chen, Qifeng Yang","doi":"10.1038/s41419-025-07580-6","DOIUrl":"10.1038/s41419-025-07580-6","url":null,"abstract":"Triple-negative breast cancer (TNBC) is characterized by a pronounced hypoxic tumor microenvironment, with cancer-associated fibroblasts (CAFs) serving as the predominant cellular component and playing crucial roles in regulating tumor progression. However, the mechanism by which CAFs affect the biological behavior of tumor cells in hypoxic environment remain elusive. This study employed a bead-based multiplex immunoassay to analyze a panel of cytokines/chemokines and identified colony stimulating factor 3 (CSF3) as a significantly elevated component in the secretome of hypoxic CAFs. We found that CSF3 promoted the invasive behavior of TNBC cells by activating the downstream signaling pathway of its receptor, CSF3R. RNA sequencing analysis further revealed that phosphoglucomutase 2-like 1 (PGM2L1) is a downstream target of the CSF3/CSF3R signaling, enhancing the glycolysis pathway and providing energy to support the malignant phenotype of breast cancer. In vivo, we further confirmed that CSF3 promotes TNBC progression by targeting PGM2L1. These findings suggest that targeting CSF3/CSF3R may represent a potential therapeutic approach for TNBC.","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"249"},"PeriodicalIF":8.1,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11971334/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction: Hypoxia-triggered ERRα acetylation enhanced its oncogenic role and promoted progression of renal cell carcinoma by coordinating autophagosome-lysosome fusion.

IF 8.1 1区生物学

Cell Death & Disease Pub Date : 2025-04-04 DOI: 10.1038/s41419-025-07493-4

Chun Feng, Demin Kong, Binghua Tong, Yonghui Liang, Fuyi Xu, Yangyang Yang, Yingying Wu, Xiaodong Chi, Pengfei Wei, Yang Yang, Guilong Zhang, Geng Tian, Zhaowei Xu

引用次数: 0

Microenvironmental control of the ductular reaction: balancing repair and disease progression.

IF 8.1 1区生物学

Cell Death & Disease Pub Date : 2025-04-04 DOI: 10.1038/s41419-025-07590-4

Giovanni Sorrentino

{"title":"Microenvironmental control of the ductular reaction: balancing repair and disease progression.","authors":"Giovanni Sorrentino","doi":"10.1038/s41419-025-07590-4","DOIUrl":"10.1038/s41419-025-07590-4","url":null,"abstract":"The ductular reaction (DR) is a dynamic adaptive cellular response within the liver, triggered by various hepatic insults and characterized by an expansion of dysmorphic biliary epithelial cells and liver progenitors. This complex response presents a dual role, playing a pivotal function in liver regeneration but, paradoxically, contributing to the progression of liver diseases, depending upon specific contextual factors and signaling pathways involved. This comprehensive review aims to offer a holistic perspective on the DR, focusing into its intricate cellular and molecular mechanisms, highlighting its pathological significance, and exploring its potential therapeutic implications. An up-to-date understanding of the DR in the context of different liver injuries is provided, analyzing its contributions to liver regeneration, inflammation, fibrosis, and ultimately carcinogenesis. Moreover, the review highlights the role of multiple microenvironmental factors, including the influence of extracellular matrix, tissue mechanics and the interplay with the intricate hepatic cell ecosystem in shaping the DR's regulation. Finally, in vitro and in vivo experimental models of the DR will be discussed, providing insights into how researchers can study and manipulate this critical cellular response. By comprehensively addressing the multifaceted nature of the DR, this review contributes to a more profound understanding of its pathophysiological role in liver diseases, thus offering potential therapeutic avenues for hepatic disorders and improving patient outcomes.","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"246"},"PeriodicalIF":8.1,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11968979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Generation and validation of a novel multitarget small molecule in glioblastoma.

IF 8.1 1区生物学

Cell Death & Disease Pub Date : 2025-04-04 DOI: 10.1038/s41419-025-07569-1

Aizpea Artetxe-Zurutuza, Nerea Iturrioz-Rodriguez, Joseba Elizazu, Mireia Toledano-Pinedo, Alicia Porro-Pérez, Irati De Goñi, Alejandro Elua-Pinin, Linda Schäker-Hübner, Mikel Azkargorta, Felix Elortza, Isabel Iriepa, Francisco Lòpez-Muñoz, Veronica Moncho-Amor, Finn K Hansen, Nicolás Sampron, Jose Luis Marco-Contelles, Ander Matheu

{"title":"Generation and validation of a novel multitarget small molecule in glioblastoma.","authors":"Aizpea Artetxe-Zurutuza, Nerea Iturrioz-Rodriguez, Joseba Elizazu, Mireia Toledano-Pinedo, Alicia Porro-Pérez, Irati De Goñi, Alejandro Elua-Pinin, Linda Schäker-Hübner, Mikel Azkargorta, Felix Elortza, Isabel Iriepa, Francisco Lòpez-Muñoz, Veronica Moncho-Amor, Finn K Hansen, Nicolás Sampron, Jose Luis Marco-Contelles, Ander Matheu","doi":"10.1038/s41419-025-07569-1","DOIUrl":"10.1038/s41419-025-07569-1","url":null,"abstract":"The development of multitarget small molecules (MSMs) has emerged as a powerful strategy for the treatment of multifactorial diseases such as cancer. Glioblastoma is the most prevalent and malignant primary brain tumor in adults, which is characterized by poor prognosis and a high heterogeneity. Current standards of treatment present limited effectiveness, as patients develop therapy resistance and recur. In this work, we synthesized and characterized a novel multi-target molecule (named DDI199 or contilistat), which is a polyfunctionalized indole derivative developed by juxtaposing selected pharmacophoric moieties of the parent compounds Contilisant and Vorinostat (SAHA) to act as multifunctional ligands that inhibit histone deacetylases (HDACs), monoamine oxidases (MAOs) and cholinesterases (ChEs), and modulate histamine H3 (H3R) and Sigma 1 Receptor (S1R) receptors. DDI199 exerts high cytotoxic activity in conventional glioblastoma cell lines and patient-derived glioma stem cells in vitro. Importantly, it significantly reduces tumor growth in vivo, both alone and in combination with temozolomide (TMZ). The comparison with SAHA showed higher target specificity and antitumor activity of the new molecule. Transcriptomic and proteomic analyses of patient-derived glioma stem cells revealed a deregulation in cell cycle, DNA remodeling and neurotransmission activity by the treatment with DDI199. In conclusion, our data reveal the efficacy of a novel MSM in glioblastoma pre-clinical setting.","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"250"},"PeriodicalIF":8.1,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11971462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RIPK2 promotes colorectal cancer metastasis by protecting YAP degradation from ITCH-mediated ubiquitination.

IF 8.1 1区生物学

Cell Death & Disease Pub Date : 2025-04-04 DOI: 10.1038/s41419-025-07599-9

Chen Lu, Hongda Liu, Tianyu Liu, Sizheng Sun, Yanan Zheng, Tao Ling, Xiagang Luo, Yiming E, Yuting Xu, Jie Li, Lei Liu, Lin Miao, Zhengxia Liu, Chunzhao Yu

{"title":"RIPK2 promotes colorectal cancer metastasis by protecting YAP degradation from ITCH-mediated ubiquitination.","authors":"Chen Lu, Hongda Liu, Tianyu Liu, Sizheng Sun, Yanan Zheng, Tao Ling, Xiagang Luo, Yiming E, Yuting Xu, Jie Li, Lei Liu, Lin Miao, Zhengxia Liu, Chunzhao Yu","doi":"10.1038/s41419-025-07599-9","DOIUrl":"10.1038/s41419-025-07599-9","url":null,"abstract":"Colorectal cancer (CRC) is the second leading cause of cancer-related death worldwide, making the exploration of metastatic mechanisms crucial for therapeutic advancements. In this study, we identified receptor-interacting protein kinase 2 (RIPK2) as an independent risk factor for poor CRC prognosis. Single-cell RNA sequencing and spatial transcriptomics revealed that a tumor cell cluster with high RIPK2 expression exhibited enhanced metastatic potential, closely linked to bacterial invasion. In vitro and in vivo experiments confirmed that RIPK2 specifically promotes tumor cell migration and invasion, rather than proliferation. Proteomic analysis indicated that RIPK2 knockdown leads to increased proteolysis mediated by ubiquitin, particularly affecting the oncoprotein YAP. Additionally, bacterial invasion of epithelial cells was significantly suppressed in RIPK2 knockdown cells, suggesting a connection to the NOD2-RIPK2 pathway, stimulated by bacterial muramyl dipeptide (MDP). We demonstrated that MDP levels are significantly higher in CRC tissues compared to adjacent non-cancerous tissues, correlating with RIPK2 activation. This activation triggers K63-linked ubiquitination of RIPK2, essential for NF-κB and MAPK pathway activation. Mechanistic studies identified the E3 ubiquitin ligase ITCH as a critical mediator, balancing K63-linked ubiquitination of RIPK2 and K48-linked ubiquitination of YAP, leading to YAP degradation and suppressed CRC metastasis. The stability of YAP could also be disrupted by GSK583, a pharmacological inhibitor of RIPK2, effectively suppressing CRC metastasis. Our findings provide deep insights into RIPK2's role in CRC progression and present a promising target for future therapeutic strategies.","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"248"},"PeriodicalIF":8.1,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11971272/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Growth factor receptor plasticity drives therapeutic persistence of metastatic breast cancer.

IF 8.1 1区生物学

Cell Death & Disease Pub Date : 2025-04-04 DOI: 10.1038/s41419-025-07591-3

Mitchell Ayers, Marvis Monteiro, Aneesha Kulkarni, Julie W Reeser, Emily Dykhuizen, Sameek Roychowdhury, Michael K Wendt

{"title":"Growth factor receptor plasticity drives therapeutic persistence of metastatic breast cancer.","authors":"Mitchell Ayers, Marvis Monteiro, Aneesha Kulkarni, Julie W Reeser, Emily Dykhuizen, Sameek Roychowdhury, Michael K Wendt","doi":"10.1038/s41419-025-07591-3","DOIUrl":"10.1038/s41419-025-07591-3","url":null,"abstract":"Metastatic breast cancer (MBC) remains a therapeutic challenge due to the persistence of minimal residual disease (MRD) and tumor recurrence. Herein we utilize a model of MBC that is sensitive to inhibition of fibroblast growth factor receptor (FGFR), resulting in robust regression of pulmonary lesions upon treatment with the FGFR inhibitor pemigatinib. Assessment of the remaining MRD revealed upregulation of platelet-derived growth factor receptor (PDGFR). Functionally, we demonstrate increased response to PDGF ligand stimulation following pemigatinib treatment. Depletion of PDGFR did not alter tumor growth under control conditions but did delay tumor recurrence following a treatment window of pemigatinib. To overcome this therapeutic hurdle, we found that inhibition of DNA methyltransferase 1 (DNMT1) prevents pemigatinib-induced cellular plasticity. Combined targeting of FGFR and DNMT1 prevented induction of PDGFR, enhanced pulmonary tumor regression, slowed tumor recurrence, and prolonged survival. These findings enhance our understanding of cellular plasticity during states of treatment-induced MRD and suggest that inhibition of DNA methylation could augment current approaches being used to treat MBC.","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"251"},"PeriodicalIF":8.1,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11971261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0