Cell Cycle最新文献

{"title":"Correction.","authors":"","doi":"10.1080/15384101.2025.2607788","DOIUrl":"10.1080/15384101.2025.2607788","url":null,"abstract":"","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"i-iii"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145809789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TCAB1: a key promoter of tumor growth through telomere maintenance and senescence evasion.","authors":"Mei-Yu Lin, Dian Jiang, Nini Tian, Xiang Yao, Xing-Hua Pan, Li-Hua Ma, Jing Gao, Zi-An Li, Xiang-Qin Zhu, Xi-Long Zhao, Guang-Ping Ruan","doi":"10.1080/15384101.2025.2609646","DOIUrl":"10.1080/15384101.2025.2609646","url":null,"abstract":"<p><p>TCAB1 (telomerase Cajal body protein 1), encoded by the WRAP53 gene on chromosome 17p13.1, is a molecular scaffold critical for protein-nucleic acid interactions. In normal cells, TCAB1 plays a pivotal role in localizing telomerase to Cajal bodies, thereby ensuring proper telomere maintenance and genomic stability. In cancer cells, however, TCAB1 is frequently overexpressed, which supports unchecked proliferation and therapy resistance. Conversely, knockdown of TCAB1 triggers multiple tumor-suppressive mechanisms, including G1 cell cycle arrest - mediated by impaired p21 ubiquitination and subsequent Cyclin E/CDK2 inactivation - as well as telomere shortening and genomic instability due to mitochondrial dysfunction and defective DNA repair. Notably, the induction of cellular senescence emerges as a key anticancer mechanism upon TCAB1 depletion, particularly in early-stage tumors retaining wild-type p53. This review delineates the dual roles of TCAB1, highlighting its function as a context-dependent oncoprotein and the therapeutic potential of targeting it to induce senescence.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-14"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145899224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Control of DNA double-strand break repair by the KDM8 histone demethylase.","authors":"Jérémie Fages, Valérie Bergoglio, Emmanuel Julia, Luana Cintori, Catherine Chailleux, Anne-Lise Fourez, Natacha Ponsolle, Didier Trouche, Yvan Canitrot","doi":"10.1080/15384101.2026.2659192","DOIUrl":"10.1080/15384101.2026.2659192","url":null,"abstract":"<p><p>KDM8 is a histone demethylase initially characterized for its activity on H3K36me2, although its function is now more widely recognized as a hydroxylase. Through a high-throughput screening on histone demethylases, we identified KDM8 as a regulator of the γH2AX response following ionizing radiation. Experiments using specific reporter substrates revealed that KDM8 depletion increases homologous recombination (HR), while its overexpression reduces HR. This shift is counterbalanced by a concomitant decrease in non-homologous end joining (NHEJ), an effect partly independent of its demethylase activity and unrelated to cell cycle alterations. Despite this imbalance, cellular sensitivity to DNA-damaging agents - such as ionizing radiation, mitomycin C, and camptothecin - remains unchanged. FRET experiments in living cells demonstrated an interaction between KDM8 and Rad51 after DNA damage induced by camptothecin. These findings identify KDM8 as a key player in DSB repair, specifically influencing HR.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-14"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13094220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitotic error correction and the spindle assembly checkpoint: a tension-filled relationship.","authors":"Richard Pleuger, Stefan Westermann","doi":"10.1080/15384101.2026.2653527","DOIUrl":"10.1080/15384101.2026.2653527","url":null,"abstract":"<p><p>The fidelity of mitotic chromosome segregation relies on kinetochores detecting sister chromatid bi-orientation to control error correction (EC) and the spindle assembly checkpoint (SAC). The kinetochore-microtubule attachment state needs to be decoded, the signal processed, and transduced, resulting in either stabilization or destabilization of the attachment. Although many crucial players of this process have been identified, the molecular mechanisms underlying signal integration remain an open question. Focusing on the model system <i>Saccharomyces cerevisiae</i>, we explore the interdependent contributions of the conserved protein kinases Mps1 and Ipl1^{Aurora B}, crucial regulators of mitotic chromosome segregation. We discuss how bi-orientation reorganizes the kinetochore attachment site and we present a perspective on how these structural changes can alter kinase localization and activity.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-19"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147608213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomes derived from AHR-overexpressing human umbilical cord mesenchymal stem cells attenuate H/R injury via AHR/NLRP3 pathway.","authors":"Ying Qin, Dongyan Shen, Kequan Guo, Xu Meng, Xiaozheng Cui, Yongchao Li, Yixin Jia","doi":"10.1080/15384101.2025.2609649","DOIUrl":"10.1080/15384101.2025.2609649","url":null,"abstract":"<p><p>Myocardial hypoxia-reoxygenation (H/R) injury is a frequently observed pathological event in various cardiovascular conditions. Despite the therapeutic promise of human umbilical cord mesenchymal stem cells (hUC-MSCs) in alleviating myocardial damage, their clinical use faces obstacles such as limited implantation efficiency, poor retention, and reduced post-transplantation viability. Exosomes secreted by hUC-MSCs have emerged as a viable alternative, potentially addressing these challenges. Nonetheless, the underlying mechanisms through which these exosomes confer cardioprotection have yet to be fully elucidated. This study aims to explore the protective effect of hUC-MSCs exosomes on myocardial H/R injury via the aryl hydrocarbon receptor (AHR)/NOD-like receptor family pyrin domain containing 3 (NLRP3) pathway and to assess their impact on immune cell phenotype conversion. hUC-MSCs exosomes significantly upregulated AHR expression, inhibited NLRP3-related inflammatory protein expression, enhanced myocardial cell survival, and reduced apoptosis. The protective effect of hUC-MSCs exosomes was abolished following AHR knockdown. Additionally, exosomes from AHR-overexpressing hUC-MSCs promoted the conversion of macrophages, dendritic cells (DCs), and T cells to an anti-inflammatory phenotype, thereby further enhancing myocardial protection. These findings indicted that exosomes from AHR-overexpressing hUC-MSCs protect myocardium via AHR/NLRP3 signaling, improving immune microenvironment and offering new therapeutic potential.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-22"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146164291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functions of exosomal microRNAs from adipose tissue in diabetes mellitus and related cardiovascular pathologies.","authors":"Yong-Zhen Li, Yu-Tao Zhang, Xiao-Hong Li","doi":"10.1080/15384101.2025.2590058","DOIUrl":"10.1080/15384101.2025.2590058","url":null,"abstract":"<p><p>Adipose tissue is central to energy homeostasis and endocrine function, and its dysregulation is a key driver of metabolic disorders. Exosomes, serving as critical intercellular messengers, mediate systemic metabolic responses by delivering bioactive cargo, including nucleic acids, proteins, and lipids. Mounting evidence identifies adipose-derived exosomes as potent mediators of obesity-related inflammation and glucose metabolic dysfunction, thereby contributing to insulin resistance and diabetic complications. This review summarizes the pivotal roles of exosomal microRNAs (miRNAs) and highlights their significant potential as a novel class of small RNA therapeutics. Unlike synthetic delivery systems, exosomal miRNAs constitute an inherent delivery vehicle that synergizes natural targeting efficiency with potent gene regulatory functions. This unique combination enables the precise coordination of complex gene networks involved in metabolic disease, offering a distinct advantage over conventional single-target approaches. Consequently, exosomal miRNAs are positioned as promising candidates for pioneering RNA-based therapies against pervasive conditions such as diabetes and cardiovascular disease.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-19"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915770/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145539285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of mitochondrial permeability transition-related gene signatures to predict lung adenocarcinoma survival and drug response.","authors":"Lin Liu, Mingjun Gao, Wenbo He, Mengmeng Wang, Siding Zhou, Xiaolin Wang, Yusheng Shu","doi":"10.1080/15384101.2025.2606113","DOIUrl":"10.1080/15384101.2025.2606113","url":null,"abstract":"<p><p>This study investigated mitochondrial permeability transition-driven necrosis-related genes (MPTDNRGs) and its association with lung adenocarcinoma (LUAD). We systematically investigated their genetic variation, expression patterns, and prognostic value. A risk prediction model for MPTDNRGs was contrasted using Cox regression and least absolute shrinkage and selection operator regression analyses. MPTDNRG scores were used to quantify LUAD subtypes. We evaluated their value in the tumor microenvironment (TME), tumor mutational burden (TMB), prognostic prediction, and drug sensitivity in LUAD. The expression level, copy number variation, methylation, and microRNA (miRNA) status of PSMB7 were analyzed. We also analyzed the expression and knockdown efficiency of PSMB7 in LUAD by immunohistochemical staining, real-time fluorescence quantitative polymerase chain reaction, and western blotting. PSMB7 function in LUAD cells and in vivo was assayed using Cell Counting Kit 8, colony formation, wound healing, Transwell assays, flow cytometry, and mouse models. Seven MPTDNRG features were successfully constructed to predict LUAD prognosis and validated in an external cohort. Patients were categorized into high- and low-risk groups based on risk scores. The high-risk group exhibited shorter survival times, lower TME scores, weaker TME cell infiltration, and higher TMB scores than the low-risk group. Cancer stem cell index, mutation frequency, and drug sensitivity significantly differed between the two groups. MPTDNRG score could independently predict LUAD. PSMB7 was highly expressed in various tumors, and copy number variation, methylation, and miRNA expression significantly differed among different cancers. PSMB7 was highly expressed in LUAD tissues and cell lines. PSMB7 knockdown inhibited cancer cell proliferation, migration, invasion, and epithelial - mesenchymal transition, and promoted apoptosis. PSMB7 exerted tumorigenic effects in mice. In conclusion, we comprehensively demonstrated the characterization of MPTDNRGs in LUAD and constructed a new risk prediction model. Meanwhile, PSMB7 was shown to be a possible new target for LUAD treatment.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-35"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145848968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction.","authors":"","doi":"10.1080/15384101.2026.2664293","DOIUrl":"https://doi.org/10.1080/15384101.2026.2664293","url":null,"abstract":"","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"2664293"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13114108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of SGK3 regulates hyperplastic scar development in rats through the MAPK/ERK signaling pathway.","authors":"Fuyong Wang, Duanxiang Wang, Weidong Wang, Huaqiang Li","doi":"10.1080/15384101.2026.2627904","DOIUrl":"10.1080/15384101.2026.2627904","url":null,"abstract":"<p><p>Hypertrophic scars (HS) frequently result from severe burns, surgical procedures and other causes of deep skin damage. The impact of serum/glucocorticoid regulated kinase family member 3 (SGK3) on the formation of HS remains unclear. HS model rats were constructed by the scalding method. In addition, tissue samples from clinical patients were collected to detect the SGK3 levels in normal skin and HS tissues by RT-qPCR and western blotting. Human-derived HS fibroblasts (HSFBs) were isolated and identified using immunofluorescence. Cell Counting Kit-8, 5-Ethynyl-2'-deoxyuridine staining and scratch assays were applied to test the ability of the HSFBs to proliferate and migrate. The influence of an SGK3 inhibitor on wound healing in rats was assessed using hematoxylin and eosin staining, Masson staining, immunofluorescence and immunohistochemistry. In addition, the levels of collagen and the proteins involved in the mitogen-activated protein kinase (MAPK)/extracellular regulated protein kinase (ERK) pathway were measured by western blotting. SGK3 was highly expressed in HS tissues. Knockdown of SGK3 resulted in reduced SGK3 levels in HSFBs. Knockdown of SGK3 reduced the proliferation and migration ability of HSFBs and suppressed cellular fibrosis. Injection with an SGK3 inhibitor reduced the burn scar area, decreased epithelial thickness and inhibited collagen deposition in rats. This inhibitor also resulted in the downregulation of collagen and MAPK/ERK pathway-related proteins. In addition, MAPK/ERK pathway agonists attenuated the effect of SGK3 inhibition, promoting HS formation while inhibiting wound healing in rats; however, MAPK inhibitors had the opposite effect. In conclusion, inhibition of SGK3 reduces the proliferation, migration and fibrosis abilities of HSFBs as well as promotes wound healing and inhibits HS formation in rats by downregulating the MAPK/ERK pathway.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-16"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146164299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of Concern: Rad18 E3 ubiquitin ligase activity mediates Fanconi anemia pathway activation and cell survival following DNA Topoisomerase 1 inhibition.","authors":"","doi":"10.1080/15384101.2026.2626210","DOIUrl":"10.1080/15384101.2026.2626210","url":null,"abstract":"","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928612/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}