Extracellular vesicles (EVs), as pivotal "messengers" in intercellular communication within the tumor microenvironment (TME), play multifaceted regulatory roles in the initiation, progression, and therapeutic response of colorectal cancer (CRC). This review focuses on the roles of EVs in CRC progression, including the creation of an immunosuppressive microenvironment and the modulation of other cells within the TME. Additionally, the article briefly discusses the potential biomarker value of EVs for early diagnosis and metastasis prediction. Furthermore, several therapeutic strategies employing EVs for CRC treatment are introduced, such as adjuvant immunotherapy, the use of stem cell-derived EVs, and engineered EVs. In this context, we emphasize the limitations and challenges of EV-based research and explore the future prospects of this field, aiming towards the realization of its practical application in the precise diagnosis and treatment of CRC.
{"title":"Extracellular vesicles cargo orchestration in colorectal cancer: immune evasion, stromal remodeling, and therapeutic frontiers.","authors":"Yukang Lu,Xiulan Liu,Tingting Zhang,Meijin Liu,Xiaoyan Liu,Jinyou Qiu,Linghan Zhang,Zhenzhen Wen","doi":"10.1186/s12943-025-02532-2","DOIUrl":"https://doi.org/10.1186/s12943-025-02532-2","url":null,"abstract":"Extracellular vesicles (EVs), as pivotal \"messengers\" in intercellular communication within the tumor microenvironment (TME), play multifaceted regulatory roles in the initiation, progression, and therapeutic response of colorectal cancer (CRC). This review focuses on the roles of EVs in CRC progression, including the creation of an immunosuppressive microenvironment and the modulation of other cells within the TME. Additionally, the article briefly discusses the potential biomarker value of EVs for early diagnosis and metastasis prediction. Furthermore, several therapeutic strategies employing EVs for CRC treatment are introduced, such as adjuvant immunotherapy, the use of stem cell-derived EVs, and engineered EVs. In this context, we emphasize the limitations and challenges of EV-based research and explore the future prospects of this field, aiming towards the realization of its practical application in the precise diagnosis and treatment of CRC.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"36 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145680570","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}
BACKGROUNDCircular RNAs (circRNAs) exert critical regulatory functions in tumor biology by modulating pathways associated with oncogenesis or tumor suppression. Despite substantial progress in elucidating their roles in several malignancies, the contribution of circRNAs to the pathogenesis of driver gene-negative lung adenocarcinoma (LUAD), a molecular subtype lacking actionable genetic alterations and exhibiting limited response to existing targeted or immunotherapeutic strategies, remains poorly defined.METHODSThe expression of circRNF10 in driver gene-negative LUAD was analyzed using circRNA microarray analysis followed by RT-qPCR validation. A series of functional assays were performed both in vitro and in vivo to evaluate the effects of circRNF10 on tumor cell behavior, including proliferation (EdU incorporation), migration (wound healing), and invasion (transwell assays), as well as tumor growth in a murine model. To elucidate the underlying molecular mechanism, we employed a combination of computational and experimental approaches, including AlphaFold3-based structural prediction, in vitro transcription, biotin-labeled RNA pulldown, RNA immunoprecipitation (RIP), and dual-luciferase reporter assays.RESULTSIn this study, we identified a previously uncharacterized circular RNA, circRNF10, which is markedly downregulated in driver gene-negative lung adenocarcinoma (LUAD) and positively associated with favorable clinical outcomes. Functional analyses revealed that circRNF10 overexpression suppresses LUAD cell proliferation, migration, and invasion in vitro and in vivo, primarily through inhibition of the Wnt/β-catenin signaling pathway. Mechanistically, circRNF10 directly interacts with β-catenin via its cyclization site, thereby promoting β-catenin degradation. Moreover, circRNF10 functions as a competing endogenous RNA by sequestering miR-1275, thereby alleviating the miR-1275-mediated suppression of DKK3, a potent inhibitor of the Wnt pathway. Our findings further confirm that circRNF10 promotes β-catenin degradation through direct interaction and modulation of the miR-1275/DKK3 signaling cascade.CONCLUSIONSCollectively, our findings highlight circRNF10 as a tumor suppressor in driver gene-negative LUAD and suggest that restoring circRNF10 expression represents a promising therapeutic approach for this refractory subtype.
{"title":"CircRNF10 sequestrates β-catenin by a dual regulatory circuit of direct degradation and a miR-1275/DKK3-mediated inhibition in driver gene- negative lung adenocarcinoma.","authors":"Xiaohua Situ,Xinwei Wang,Xiting Liao,Xiaoxuan Zhang,Sicheng Chen,Fei Fang,Lihong Wei,Peng Wu,Zhiyu Liu,Honglei Chen,Kejing Tang,Lihong Bai,Zunfu Ke","doi":"10.1186/s12943-025-02530-4","DOIUrl":"https://doi.org/10.1186/s12943-025-02530-4","url":null,"abstract":"BACKGROUNDCircular RNAs (circRNAs) exert critical regulatory functions in tumor biology by modulating pathways associated with oncogenesis or tumor suppression. Despite substantial progress in elucidating their roles in several malignancies, the contribution of circRNAs to the pathogenesis of driver gene-negative lung adenocarcinoma (LUAD), a molecular subtype lacking actionable genetic alterations and exhibiting limited response to existing targeted or immunotherapeutic strategies, remains poorly defined.METHODSThe expression of circRNF10 in driver gene-negative LUAD was analyzed using circRNA microarray analysis followed by RT-qPCR validation. A series of functional assays were performed both in vitro and in vivo to evaluate the effects of circRNF10 on tumor cell behavior, including proliferation (EdU incorporation), migration (wound healing), and invasion (transwell assays), as well as tumor growth in a murine model. To elucidate the underlying molecular mechanism, we employed a combination of computational and experimental approaches, including AlphaFold3-based structural prediction, in vitro transcription, biotin-labeled RNA pulldown, RNA immunoprecipitation (RIP), and dual-luciferase reporter assays.RESULTSIn this study, we identified a previously uncharacterized circular RNA, circRNF10, which is markedly downregulated in driver gene-negative lung adenocarcinoma (LUAD) and positively associated with favorable clinical outcomes. Functional analyses revealed that circRNF10 overexpression suppresses LUAD cell proliferation, migration, and invasion in vitro and in vivo, primarily through inhibition of the Wnt/β-catenin signaling pathway. Mechanistically, circRNF10 directly interacts with β-catenin via its cyclization site, thereby promoting β-catenin degradation. Moreover, circRNF10 functions as a competing endogenous RNA by sequestering miR-1275, thereby alleviating the miR-1275-mediated suppression of DKK3, a potent inhibitor of the Wnt pathway. Our findings further confirm that circRNF10 promotes β-catenin degradation through direct interaction and modulation of the miR-1275/DKK3 signaling cascade.CONCLUSIONSCollectively, our findings highlight circRNF10 as a tumor suppressor in driver gene-negative LUAD and suggest that restoring circRNF10 expression represents a promising therapeutic approach for this refractory subtype.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"46 5 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145680571","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}
This study developed and validated a diagnostic signature comprising five small extracellular vesicle (sEV)-derived long RNAs (ATF4, GRAP2, MCL1, PAK2, PIK3CB) for distinguishing early-stage lung adenocarcinoma (LUAD) from benign pulmonary nodules and assessing prognosis in advanced LUAD. Utilizing a multi-center cohort of 698 participants, researchers employed RNA sequencing and quantitative PCR to analyze plasma sEV RNA profiles. Differentially expressed mRNAs and long intergenic non-coding RNAs (lincRNAs) were identified using LASSO regression to construct a diagnostic model. The signature demonstrated high diagnostic accuracy with an area under the curve (AUC) of 0.971 in the validation cohort and 0.950 in the prospective cohort. It also surpassed low-dose CT sensitivity (95.24% vs. 71.43%), specificity (100% vs. 93.96%), positive predictive value (100% vs. 45.45%) and negative predictive value (99.67% vs. 97.90%) in the prospective cohort. In advanced LUAD patients undergoing chemoradiotherapy or PD-L1 inhibitor therapy, lower expression of these RNAs correlated with improved progression-free survival (PFS; HR = 0.38-0.39). The signature integrates non-invasively detected sEV RNAs to complement LDCT, addressing its high false-positive rate, and offers prognostic insights for personalized treatment strategies. These findings highlight the clinical potential of sEV-derived long RNAs in early LUAD detection and precision oncology.
{"title":"Development and validation of a small extracellular vesicle-derived RNA signature for early diagnosis of lung adenocarcinoma and prognosis in advanced stages.","authors":"Rui Meng,Yanjun Gao,Zheng Peng,Hua Chen,Yida Li,Yu Liu,Lanxiao Shen,Huanle Pan,Liangcheng Zheng,Dezhi Cheng,Xiaoming Lin,Wenjie Sun,Congying Xie","doi":"10.1186/s12943-025-02524-2","DOIUrl":"https://doi.org/10.1186/s12943-025-02524-2","url":null,"abstract":"This study developed and validated a diagnostic signature comprising five small extracellular vesicle (sEV)-derived long RNAs (ATF4, GRAP2, MCL1, PAK2, PIK3CB) for distinguishing early-stage lung adenocarcinoma (LUAD) from benign pulmonary nodules and assessing prognosis in advanced LUAD. Utilizing a multi-center cohort of 698 participants, researchers employed RNA sequencing and quantitative PCR to analyze plasma sEV RNA profiles. Differentially expressed mRNAs and long intergenic non-coding RNAs (lincRNAs) were identified using LASSO regression to construct a diagnostic model. The signature demonstrated high diagnostic accuracy with an area under the curve (AUC) of 0.971 in the validation cohort and 0.950 in the prospective cohort. It also surpassed low-dose CT sensitivity (95.24% vs. 71.43%), specificity (100% vs. 93.96%), positive predictive value (100% vs. 45.45%) and negative predictive value (99.67% vs. 97.90%) in the prospective cohort. In advanced LUAD patients undergoing chemoradiotherapy or PD-L1 inhibitor therapy, lower expression of these RNAs correlated with improved progression-free survival (PFS; HR = 0.38-0.39). The signature integrates non-invasively detected sEV RNAs to complement LDCT, addressing its high false-positive rate, and offers prognostic insights for personalized treatment strategies. These findings highlight the clinical potential of sEV-derived long RNAs in early LUAD detection and precision oncology.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"20 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145657026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-03DOI: 10.1186/s12943-025-02521-5
Hengshuo Liu,Xingyu Xiong,Weizhen Zhu,Sheng Wang,Weichao Huang,Guoqing Zhu,Hang Xu,Lu Yang
Gut microbiota-derived metabolites are emerging as systemic "remote immunoregulators" that shape tumor immunity across tissues. Integrating evidence across short-chain fatty acids, tryptophan derivatives, secondary bile acids, polyamines and other metabolites, we advance a metabolite-immune pathway-cancer framework that links receptor-mediated signaling, epigenetic remodeling and metabolic reprogramming to context-dependent, bidirectional immune effects. Importantly, in addition to the g protein-coupled receptor / aryl hydrocarbon receptor pathway, the selected microbial small molecule metabolites are the true T-cell receptor ligands of unconventional T cells, directly shaping the tissue resident immune and tumor microenvironment, supplementing the receptor signaling and epigenetic programs in our framework. We synthesize how these metabolites recalibrate the tumor immune microenvironment-modulating antigen presentation, T-cell effector fitness and exhaustion, regulatory T-cell activity, and myeloid polarization-and why the same metabolite can either potentiate immune surveillance or entrench immunosuppression depending on ligand-receptor pairing, dose and tissue niche. We compare tumor-type specific patterns (e.g., colorectal, liver, lung, breast and prostate cancers) to highlight common circuits and organ-restricted idiosyncrasies. Methodologically, we outline how single-cell and spatial multi-omics, imaging mass spectrometry and functional biosensors now enable co-registration of metabolite exposure with immune-cell states in human tumors, providing an actionable basis for biomarker discovery. Given ongoing debate about signals attributed to intratumoral microbiota in low-biomass tumor tissues, we foreground quantifiable, spatially mappable and pharmacologically tractable metabolite-receptor pathways, using microbe-associated molecular patterns / translocation as comparators to judge when chemical signals should be prioritized as intervention targets. Finally, we evaluate precision intervention avenues-including fecal microbiota transplantation, rational bacterial consortia, engineered microbes and nanoparticle-enabled metabolite delivery-and propose stratification rules that pair metabolite/receptor signatures with fit-for-purpose delivery. Together, mapping tissue-specific metabolite-immune circuits and embedding them in robust biomarker frameworks may convert microbial metabolites from correlative markers into therapeutic targets and tools, improving the efficacy and durability of cancer immunotherapy.
{"title":"Gut microbial metabolites in cancer immunomodulation.","authors":"Hengshuo Liu,Xingyu Xiong,Weizhen Zhu,Sheng Wang,Weichao Huang,Guoqing Zhu,Hang Xu,Lu Yang","doi":"10.1186/s12943-025-02521-5","DOIUrl":"https://doi.org/10.1186/s12943-025-02521-5","url":null,"abstract":"Gut microbiota-derived metabolites are emerging as systemic \"remote immunoregulators\" that shape tumor immunity across tissues. Integrating evidence across short-chain fatty acids, tryptophan derivatives, secondary bile acids, polyamines and other metabolites, we advance a metabolite-immune pathway-cancer framework that links receptor-mediated signaling, epigenetic remodeling and metabolic reprogramming to context-dependent, bidirectional immune effects. Importantly, in addition to the g protein-coupled receptor / aryl hydrocarbon receptor pathway, the selected microbial small molecule metabolites are the true T-cell receptor ligands of unconventional T cells, directly shaping the tissue resident immune and tumor microenvironment, supplementing the receptor signaling and epigenetic programs in our framework. We synthesize how these metabolites recalibrate the tumor immune microenvironment-modulating antigen presentation, T-cell effector fitness and exhaustion, regulatory T-cell activity, and myeloid polarization-and why the same metabolite can either potentiate immune surveillance or entrench immunosuppression depending on ligand-receptor pairing, dose and tissue niche. We compare tumor-type specific patterns (e.g., colorectal, liver, lung, breast and prostate cancers) to highlight common circuits and organ-restricted idiosyncrasies. Methodologically, we outline how single-cell and spatial multi-omics, imaging mass spectrometry and functional biosensors now enable co-registration of metabolite exposure with immune-cell states in human tumors, providing an actionable basis for biomarker discovery. Given ongoing debate about signals attributed to intratumoral microbiota in low-biomass tumor tissues, we foreground quantifiable, spatially mappable and pharmacologically tractable metabolite-receptor pathways, using microbe-associated molecular patterns / translocation as comparators to judge when chemical signals should be prioritized as intervention targets. Finally, we evaluate precision intervention avenues-including fecal microbiota transplantation, rational bacterial consortia, engineered microbes and nanoparticle-enabled metabolite delivery-and propose stratification rules that pair metabolite/receptor signatures with fit-for-purpose delivery. Together, mapping tissue-specific metabolite-immune circuits and embedding them in robust biomarker frameworks may convert microbial metabolites from correlative markers into therapeutic targets and tools, improving the efficacy and durability of cancer immunotherapy.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"1 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145663941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-03DOI: 10.1186/s12943-025-02539-9
Zaira Ianniello, Huimei Lu, Elias Quijano, Daniel A Colón-Ríos, Madison Rackear, Venu Bommireddy, Dale L Ludwig, Zhiyuan Shen, Peter M Glazer
{"title":"Correction: Harnessing ExDNA for precision Exatecan delivery in cancer: a novel antibody-drug conjugate approach.","authors":"Zaira Ianniello, Huimei Lu, Elias Quijano, Daniel A Colón-Ríos, Madison Rackear, Venu Bommireddy, Dale L Ludwig, Zhiyuan Shen, Peter M Glazer","doi":"10.1186/s12943-025-02539-9","DOIUrl":"10.1186/s12943-025-02539-9","url":null,"abstract":"","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"24 1","pages":"304"},"PeriodicalIF":33.9,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12673787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145669026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-02DOI: 10.1186/s12943-025-02514-4
Mingchao Xie,Miljenka Vuko,Shashank Saran,Siyu Liu,Andrew G Chambers,Hana Baakza,Helen K Angell,Felicia Ng,Carl M Gay,Robert J Cardnell,Felix J Segerer,Alma Andoni,Jaime Rodriguez-Canales,Paul M Waring,Markus Schick,J Carl Barrett,Lauren A Byers,Giulia Fabbri
BACKGROUNDGreater understanding of differential therapeutic sensitivity, specifically to immunotherapy, in small-cell lung cancer (SCLC) is required.METHODSWe explored SCLC heterogeneity through integrated molecular characterization of tumor tissue samples from 159 treatment-naive patients, utilizing genetic, epigenetic, transcriptional, and proteomic profiling, immunohistochemistry staining for multiple biologically relevant markers including transcriptional subtype-defining proteins, and spatial immune profiling using multiplex immunofluorescence.RESULTSMulti-omics analysis confirmed high heterogeneity across/within neuroendocrine and non-neuroendocrine subtypes. Methylomics analysis identified four methylome clusters that may enhance subtype prediction, prognosis, and longitudinal monitoring of subtype evolution. Immunohistochemistry analysis showed high MHC-I expression in non-neuroendocrine subtypes, which have greatest potential benefit from adding immunotherapy to chemotherapy; high DLL3 expression associated with neuroendocrine subtypes and an immune-cold tumor microenvironment. Multiplex immunofluorescence demonstrated associations of MHC-I with spatial arrangement and phenotypic features of immune cells in the tumor microenvironment of high-MHC-I-expressing SCLC, providing mechanistic rationale for MHC-I as a potential biomarker of immunotherapy response.CONCLUSIONSThis multimodal profiling analysis provides further insights into the biologic complexity of SCLC and highlights potential therapeutic vulnerabilities of distinct disease subtypes.
{"title":"Multi-omic profiling provides insights into the heterogeneity, microenvironmental features, and biomarker landscape of small-cell lung cancer.","authors":"Mingchao Xie,Miljenka Vuko,Shashank Saran,Siyu Liu,Andrew G Chambers,Hana Baakza,Helen K Angell,Felicia Ng,Carl M Gay,Robert J Cardnell,Felix J Segerer,Alma Andoni,Jaime Rodriguez-Canales,Paul M Waring,Markus Schick,J Carl Barrett,Lauren A Byers,Giulia Fabbri","doi":"10.1186/s12943-025-02514-4","DOIUrl":"https://doi.org/10.1186/s12943-025-02514-4","url":null,"abstract":"BACKGROUNDGreater understanding of differential therapeutic sensitivity, specifically to immunotherapy, in small-cell lung cancer (SCLC) is required.METHODSWe explored SCLC heterogeneity through integrated molecular characterization of tumor tissue samples from 159 treatment-naive patients, utilizing genetic, epigenetic, transcriptional, and proteomic profiling, immunohistochemistry staining for multiple biologically relevant markers including transcriptional subtype-defining proteins, and spatial immune profiling using multiplex immunofluorescence.RESULTSMulti-omics analysis confirmed high heterogeneity across/within neuroendocrine and non-neuroendocrine subtypes. Methylomics analysis identified four methylome clusters that may enhance subtype prediction, prognosis, and longitudinal monitoring of subtype evolution. Immunohistochemistry analysis showed high MHC-I expression in non-neuroendocrine subtypes, which have greatest potential benefit from adding immunotherapy to chemotherapy; high DLL3 expression associated with neuroendocrine subtypes and an immune-cold tumor microenvironment. Multiplex immunofluorescence demonstrated associations of MHC-I with spatial arrangement and phenotypic features of immune cells in the tumor microenvironment of high-MHC-I-expressing SCLC, providing mechanistic rationale for MHC-I as a potential biomarker of immunotherapy response.CONCLUSIONSThis multimodal profiling analysis provides further insights into the biologic complexity of SCLC and highlights potential therapeutic vulnerabilities of distinct disease subtypes.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"119 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145657046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01DOI: 10.1186/s12943-025-02520-6
Yansheng Wu, Hao Li, Kai Yue, Chao Jing, Yuansheng Duan
Ferroptosis is a form of cell death, distinct from apoptosis, necrosis and autophagy. It is a novel programmed cell death (PCD) triggered by iron accumulation and peroxidation associated with intracellular iron metabolism disorders. Since its naming in 2012, ferroptosis has garnered increasing attention for its role in human diseases, particularly in tumor formation, progression and therapy. Numerous studies have demonstrated that ferroptosis plays a crucial role in killing tumor cells, inhibiting tumor proliferation and metastasis and reversing therapy resistance. Consequently, targeted induction of ferroptosis in tumor cells holds promise as a novel antitumor therapeutic strategy.
{"title":"Ferroptosis in cancer: metabolism, mechanisms and therapeutic prospects.","authors":"Yansheng Wu, Hao Li, Kai Yue, Chao Jing, Yuansheng Duan","doi":"10.1186/s12943-025-02520-6","DOIUrl":"10.1186/s12943-025-02520-6","url":null,"abstract":"<p><p>Ferroptosis is a form of cell death, distinct from apoptosis, necrosis and autophagy. It is a novel programmed cell death (PCD) triggered by iron accumulation and peroxidation associated with intracellular iron metabolism disorders. Since its naming in 2012, ferroptosis has garnered increasing attention for its role in human diseases, particularly in tumor formation, progression and therapy. Numerous studies have demonstrated that ferroptosis plays a crucial role in killing tumor cells, inhibiting tumor proliferation and metastasis and reversing therapy resistance. Consequently, targeted induction of ferroptosis in tumor cells holds promise as a novel antitumor therapeutic strategy.</p>","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"24 1","pages":"303"},"PeriodicalIF":33.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12667084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145655016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-29DOI: 10.1186/s12943-025-02522-4
Do Young Hyeon, Dowoon Nam, Hye-Jin Shin, Juhee Jeong, Eunsoo Jung, Soo Young Cho, Dong Hoon Shin, Ja-Lok Ku, Hye Jung Baek, Chong Woo Yoo, Eun-Kyung Hong, Myong Cheol Lim, Sang-Jin Lee, Young-Ki Bae, Jong Kwang Kim, Jingi Bae, Wonyoung Choi, Su-Jin Kim, Seunghoon Back, Chaewon Kang, Inamul Hasan Madar, Hokeun Kim, Suhwan Kim, Duk Ki Kim, Jihyung Kang, Geon Woo Park, Ki Seok Park, Yourae Shin, Sang Soo Kim, Keehoon Jung, Daehee Hwang, Sang-Won Lee, Joo-Young Kim
{"title":"Correction: Proteogenomic characterization of molecular and cellular targets for treatment‑resistant subtypes in locally advanced cervical cancers.","authors":"Do Young Hyeon, Dowoon Nam, Hye-Jin Shin, Juhee Jeong, Eunsoo Jung, Soo Young Cho, Dong Hoon Shin, Ja-Lok Ku, Hye Jung Baek, Chong Woo Yoo, Eun-Kyung Hong, Myong Cheol Lim, Sang-Jin Lee, Young-Ki Bae, Jong Kwang Kim, Jingi Bae, Wonyoung Choi, Su-Jin Kim, Seunghoon Back, Chaewon Kang, Inamul Hasan Madar, Hokeun Kim, Suhwan Kim, Duk Ki Kim, Jihyung Kang, Geon Woo Park, Ki Seok Park, Yourae Shin, Sang Soo Kim, Keehoon Jung, Daehee Hwang, Sang-Won Lee, Joo-Young Kim","doi":"10.1186/s12943-025-02522-4","DOIUrl":"10.1186/s12943-025-02522-4","url":null,"abstract":"","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"24 1","pages":"301"},"PeriodicalIF":33.9,"publicationDate":"2025-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12664262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145636186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-29DOI: 10.1186/s12943-025-02535-z
Ariel Km Chow, Nathan Sm Cheng, Colin Sc Lam, Lui Ng, Sunny Km Wong, Timothy Mh Wan, Johnny Hw Man, Alvin Hk Cheung, Thomas Cc Yau, Jensen Tc Poon, Wai-Lun Law, Roberta Wc Pang
{"title":"Retraction Note: Preclinical analysis of the anti-tumor and anti-metastatic effects of Raf265 on colon cancer cells and CD26<sup>+</sup> cancer stem cells in colorectal carcinoma.","authors":"Ariel Km Chow, Nathan Sm Cheng, Colin Sc Lam, Lui Ng, Sunny Km Wong, Timothy Mh Wan, Johnny Hw Man, Alvin Hk Cheung, Thomas Cc Yau, Jensen Tc Poon, Wai-Lun Law, Roberta Wc Pang","doi":"10.1186/s12943-025-02535-z","DOIUrl":"10.1186/s12943-025-02535-z","url":null,"abstract":"","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"24 1","pages":"302"},"PeriodicalIF":33.9,"publicationDate":"2025-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12664263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145636137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-28DOI: 10.1186/s12943-025-02518-0
Alicia K Fleming Martinez,Heike R Döppler,Ryan Argo,Ligia I Bastea,Brandy H Edenfield,Irene Espositio,Peter Storz
{"title":"Downregulation of Sod2 increases atypical flat lesions and dysplasia to advance pancreatic ductal adenocarcinoma.","authors":"Alicia K Fleming Martinez,Heike R Döppler,Ryan Argo,Ligia I Bastea,Brandy H Edenfield,Irene Espositio,Peter Storz","doi":"10.1186/s12943-025-02518-0","DOIUrl":"https://doi.org/10.1186/s12943-025-02518-0","url":null,"abstract":"","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"90 1","pages":"300"},"PeriodicalIF":37.3,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145613345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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