Carcinogenesis最新文献

{"title":"The Tumour Neurotone: neurochemical regulation of cancer progression and therapy.","authors":"Isaac Aguirre-Maldonado, Josué Jonatan Pichardo-Espino, Julio Isael Pérez-Carreón, Alfonso Alexander-Aguilera, Luis Martínez-Paez, Fernanda Villarruel-Melquiades, Luis Del Pozo-Yauner, Claudia M García-Cuellar, Yesennia Sánchez-Pérez, Javier Camacho","doi":"10.1093/carcin/bgag076","DOIUrl":"https://doi.org/10.1093/carcin/bgag076","url":null,"abstract":"<p><p>Neural regulation of cancer extends beyond anatomical innervation: tumours receive systemic neural and neuroendocrine inputs and locally produce and decode neurotransmitters and neuropeptides. We propose the Tumour Neurotone (TN) as a tumour-level state of neurochemical regulation generated by the combined actions of these signals across malignant, immune, stromal and vascular compartments, shaping proliferative signalling, metabolic adaptation, immune escape, tissue remodelling, dissemination and treatment response. Biologically, a TN state reflects the context-dependent, spatially organised and relatively persistent configuration of neuroactive ligand availability; cell-type-specific signalling competence, including receptors, transporters and metabolic enzymes; proximal pathway engagement; and downstream cellular responses. TN is therefore not synonymous with tumour innervation, nerve density, an instantaneous neurochemical profile, neuroimmune crosstalk or the broader field of cancer neuroscience; it is a narrower state model intended to capture functional organisation beyond any single neurotransmitter pathway. We synthesise evidence across proliferative signalling, metabolic plasticity, immune regulation, sensory-neuropeptide circuits, neural remodelling, bioelectrical communication, vasculo-stromal organisation and circadian timing. Although many constituent mechanisms are causally supported, the existence and predictive value of integrated TN states have not yet been validated clinically. We therefore specify three criteria for assigning a TN state: temporal reproducibility, predictive value beyond individual components and established tumour covariates, and coherent change after targeted perturbation. We also provide a longitudinal experimental workflow, framework-specific predictions and falsification criteria, and an evidence-graded appraisal of neuromodulatory interventions.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149147582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Notice: STAT3 induces anoikis resistance, promotes cell invasion and metastatic potential in pancreatic cancer cells.","authors":"","doi":"10.1093/carcin/bgag064","DOIUrl":"https://doi.org/10.1093/carcin/bgag064","url":null,"abstract":"","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148910946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Notice: Hepatocyte growth factor-activated NF-KB regulates HIF-1 activity and ODC expression, implicated in survival, differently in different carcinoma cell lines.","authors":"","doi":"10.1093/carcin/bgag061","DOIUrl":"https://doi.org/10.1093/carcin/bgag061","url":null,"abstract":"","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PHB2 Promotes Glycolytic Reprogramming in Triple-Negative Breast Cancer Through FOXM1-Dependent Activation of LDHB.","authors":"Zankai Wu, Shanshan Wang, Qingfeng Yang, Yiping Gong, Qibin Song, Jin Hu","doi":"10.1093/carcin/bgag066","DOIUrl":"https://doi.org/10.1093/carcin/bgag066","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) presents significant clinical challenges due to its aggressive phenotype and the limited availability of molecularly targeted therapies. In this study, we investigated the therapeutic potential of targeting PHB2 in TNBC by combining bioinformatics analysis with comprehensive in vitro and in vivo experiments (CCK-8, colony formation and Transwell migration assays) to evaluate the clinical significance of PHB2 and its role in regulating the malignant phenotypes of TNBC cells. To dissect the underlying molecular circuitry, we measured glycolytic flux through glucose uptake and lactate production assays, mapped transcription-factor occupancy by chromatin immunoprecipitation (ChIP), and assessed promoter activity using dual-luciferase reporters. We demonstrate that elevated PHB2 expression leads to unfavorable prognosis in TNBC. Mechanistically, PHB2 drives glycolytic reprogramming by enhancing FOXM1-mediated transcriptional activation of LDHB, a key enzyme in anaerobic glycolysis. These findings highlight PHB2 as a critical regulator of metabolic adaptation and aggressiveness in TNBC, positioning it as a promising candidate for targeted therapy.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148910935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction of: HGF induces CXCR4 and CXCL12-mediated tumor invasion through Ets1 and NF-κB.","authors":"","doi":"10.1093/carcin/bgag046","DOIUrl":"https://doi.org/10.1093/carcin/bgag046","url":null,"abstract":"","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction of: Nuclear localization of active HGF receptor Met in aggressive MDA-MB231 breast carcinoma cells.","authors":"","doi":"10.1093/carcin/bgag045","DOIUrl":"https://doi.org/10.1093/carcin/bgag045","url":null,"abstract":"","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The P2X7 Receptor in Cancer: From Functional Receptor to Non-Functional P2X7.","authors":"Luyao Liu, Yoshiteru Kagawa, Colin L Masters, Stanley S Stylli, Julian A Barden, Theo Mantamadiotis, Ben J Gu","doi":"10.1093/carcin/bgag050","DOIUrl":"https://doi.org/10.1093/carcin/bgag050","url":null,"abstract":"<p><p>The ATP-gated P2X7 receptors are abundantly expressed in immune cells, neurons, glial cells, and cancer cells. The P2X7 receptor performs distinct functions, depending on the extracellular ATP concentration and the duration of exposure to ATP. With brief ATP stimulation, the P2X7 receptor acts as an ion channel, and the movement of ions is associated with the regulation of cell proliferation and differentiation. Prolonged ATP exposure induces a conformational change in P2X7, allowing large molecules to pass through the membrane via the formation of macropores, thereby contributing to cell death. A novel function of P2X7 as a scavenger receptor was recently reported in the absence of both serum and ATP. However, the discovery of non-functional P2X7 in cancer reveals that this group of isoforms of P2X7 fails to form macropores upon ATP stimulation and cannot initiate ATP-induced cell death, allowing malignant cells to evade this regulatory mechanism and continue proliferating. We discuss the multifaceted functions of the P2X7 receptor in regulating diverse cell types, including cell growth, death, and clearance, and how the non-functional form of P2X7 disrupts this balance in cancer. Furthermore, the review explores the potential targeting of this aberrant isoform of P2X7 in the development of novel cancer therapies.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of Concern: The interplay between hypoxia, endothelial and melanoma cells regulates vascularization and cell motility through endothelin-1 and vascular endothelial growth factor.","authors":"","doi":"10.1093/carcin/bgag048","DOIUrl":"https://doi.org/10.1093/carcin/bgag048","url":null,"abstract":"","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editor's Note: Overexpression of Cdc20 leads to impairment of the spindle assembly checkpoint and aneuploidization in oral cancer.","authors":"","doi":"10.1093/carcin/bgag023","DOIUrl":"https://doi.org/10.1093/carcin/bgag023","url":null,"abstract":"","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editor's Note: FAK and IGF-IR interact to provide survival signals in human pancreatic adenocarcinoma cells.","authors":"","doi":"10.1093/carcin/bgag042","DOIUrl":"10.1093/carcin/bgag042","url":null,"abstract":"","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}