Cell Cycle最新文献_第7页

Repurposing the anti-gout drug benzbromarone for the treatment of glioma. 将抗痛风药物苯溴马龙用于治疗神经胶质瘤。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2025-11-07 DOI: 10.1080/15384101.2025.2587234

Mengmeng Huo, Ziwei Wang, Wanying Guo, Jun Gong, Helin Lu, Wu Liu, Liqiong Ding

{"title":"Repurposing the anti-gout drug benzbromarone for the treatment of glioma.","authors":"Mengmeng Huo, Ziwei Wang, Wanying Guo, Jun Gong, Helin Lu, Wu Liu, Liqiong Ding","doi":"10.1080/15384101.2025.2587234","DOIUrl":"10.1080/15384101.2025.2587234","url":null,"abstract":"Glioma has long been a threat to human health and new treatments are required to address this health problem. We here explored the potential use of benzbromarone as a supplement to existing chemotherapy strategies. The effects of benzbromarone on the proliferation and migration of C6 glioma cells were evaluated by MTT and wound healing assays. The effects of benzbromarone on cell cycle arrest and apoptosis in C6 glioma cells were determined by flow cytometry. The effect of benzbromarone on reactive oxygen species (ROS) production was determined through fluorescence microscopy and flow cytometry. Finally, the effect of benzbromarone on the NF-κB pathway was determined by western blotting and immunofluorescence. Benzbromarone inhibited the growth and migration of C6 glioma cells in a concentration-dependent manner. Benzbromarone also induced cell cycle arrest and apoptosis in C6 glioma cells, in addition to increasing ROS generation. Western blot analysis revealed that benzbromarone activated the NF-κB signaling pathway. Our results suggest that benzbromarone induces cytotoxicity through ROS production. These findings indicate the potential of benzbromarone as a treatment of glioma.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-12"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915828/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145457705","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}

引用次数: 0

Targeting IMPDH to inhibit SAMHD1 in KMT2A-rearranged leukaemia. 靶向IMPDH抑制kmt2a重排白血病中的SAMHD1。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2025-12-15 DOI: 10.1080/15384101.2025.2601796

Yolande Klootsema, Nikolaos Tsesmetzis, Sushma Sharma, Sophia Hofmann, Jonas Thier, Christopher Dirks, Femke M Hormann, Miriam Yagüe-Capilla, Anna Bohlin, Sofia Bengtzen, Sören Lehmann, Andrei Chabes, Martin Jädersten, Vanessa Lundin, Sean G Rudd, Ingrid Lilienthal, Nikolas Herold

{"title":"Targeting IMPDH to inhibit SAMHD1 in KMT2A-rearranged leukaemia.","authors":"Yolande Klootsema, Nikolaos Tsesmetzis, Sushma Sharma, Sophia Hofmann, Jonas Thier, Christopher Dirks, Femke M Hormann, Miriam Yagüe-Capilla, Anna Bohlin, Sofia Bengtzen, Sören Lehmann, Andrei Chabes, Martin Jädersten, Vanessa Lundin, Sean G Rudd, Ingrid Lilienthal, Nikolas Herold","doi":"10.1080/15384101.2025.2601796","DOIUrl":"10.1080/15384101.2025.2601796","url":null,"abstract":"Cytarabine (ara-C) and fludarabine (F-ara-A) are key drugs in leukaemia treatment. SAMHD1 is known to confer resistance to ara-C and F-ara-A, and we previously identified ribonucleotide reductase inhibitors as indirect SAMHD1 inhibitors in a phenotypic screen. The inosine monophosphate dehydrogenase (IMPDH) inhibitor mycophenolic acid (MPA) was also a hit in this screen. IMPDH inhibitors (IMPDHi) have previously shown efficacy against KMT2A-rearranged (KMT2Ar) acute myeloid leukaemia (AML). We investigated whether IMPDH inhibition could enhance the effect of ara-C and F-ara-A in AML cell lines and primary AML samples, and whether this effect was linked to KMT2A status. We found that sensitivity to IMPDHi was independent of KMT2A status. IMPDHi synergized with ara-C and F-ara-A in a SAMHD1-dependent manner in a subset of AML cells, but not in acute lymphoblastic leukaemia cell lines. Mechanistically, IMPDHi depleted allosteric SAMHD1 activators GTP and dGTP, thereby increasing active triphosphate metabolites in SAMHD1-proficient, but not SAMHD1-deficient, cells. Our findings suggest that the addition of IMPDHi to ara-C and F-ara-A may have therapeutic benefits in some AML cases.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-19"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145762405","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}

引用次数: 0

Identification of PGF+ endothelial cells associated with plaque instability in carotid atherosclerosis by scRNA-seq and RNA-seq analysis. 通过scRNA-seq和RNA-seq分析鉴定颈动脉粥样硬化斑块不稳定相关的PGF+内皮细胞。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-06-28 DOI: 10.1080/15384101.2026.2688663

Yi Xiang, Dong Liu, Wenwen Jin, Tao Xu, Leilei Guo, Tingchun Wu, Yuhua Zheng, Xiaoman Xiong, Haixia Xiong, Hua He

{"title":"Identification of PGF+ endothelial cells associated with plaque instability in carotid atherosclerosis by scRNA-seq and RNA-seq analysis.","authors":"Yi Xiang, Dong Liu, Wenwen Jin, Tao Xu, Leilei Guo, Tingchun Wu, Yuhua Zheng, Xiaoman Xiong, Haixia Xiong, Hua He","doi":"10.1080/15384101.2026.2688663","DOIUrl":"10.1080/15384101.2026.2688663","url":null,"abstract":"Vascular endothelial dysfunction plays a critical role in the development of atherosclerosis; however, the mechanisms by which endothelial cells contribute to plaque instability remain incompletely understood. In this study, we performed an integrated analysis of single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data to characterize endothelial cell heterogeneity associated with carotid plaque instability. Clustering analysis, gene set variation analysis (GSVA), differential gene expression analysis, and KEGG pathway enrichment were conducted to identify key endothelial cell subsets and their functional characteristics. We identified three endothelial cell subsets (subsets 9, 10, and 11) that were significantly enriched in unstable plaques and exhibited upregulation of multiple pro-inflammatory cytokines. Pathway analysis revealed that these subsets were associated with activation of the PI3K - Akt signaling pathway and other inflammation-related pathways. Furthermore, findings were validated in an apolipoprotein E-deficient (ApoE-/-) mouse model, where increased expression of placental growth factor (PGF) and a higher proportion of PGF-positive endothelial cells were observed in atherosclerotic lesions. In conclusion, this study reveals the heterogeneity of endothelial cells in atherosclerotic plaques and identifies pro-inflammatory endothelial subsets potentially associated with plaque instability, providing new insights into the pathogenesis of atherosclerosis.Trial registration: This study was approved by the Experimental Animal Ethics Committee of Guizhou University of Chinese Medicine (approval number: 2,024,010).","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-20"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13313253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148337592","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}

引用次数: 0

CTDSPL2 facilitates resistance to paclitaxel in breast cancer cells by suppressing SCYL1 phosphorylation. CTDSPL2通过抑制SCYL1磷酸化促进乳腺癌细胞对紫杉醇的抗性。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-04-27 DOI: 10.1080/15384101.2026.2663187

Jing Zhao, Wei Zhao, Zhimin Wei, Feng Hou, Lingling Sun, Xia Li, Xianning Dong

{"title":"CTDSPL2 facilitates resistance to paclitaxel in breast cancer cells by suppressing SCYL1 phosphorylation.","authors":"Jing Zhao, Wei Zhao, Zhimin Wei, Feng Hou, Lingling Sun, Xia Li, Xianning Dong","doi":"10.1080/15384101.2026.2663187","DOIUrl":"10.1080/15384101.2026.2663187","url":null,"abstract":"Breast cancer (BC) exhibits significant heterogeneity and complexity and is leading causes of mortality in women globally. Paclitaxel (PTX) is commonly utilized as the primary medication for BC. However, the resistance of BC to PTX poses a significant challenge in clinical treatment. This study aimed at to explore whether carboxy-terminal domain small phosphatase like 2 (CTDSPL2) affected PTX resistance in BC cells. PTX resistant BC cell lines, including MCF-7/PTX and MDA-MB-231/PTX, were developed by continuously increasing PTX concentration, and we found that CTDSPL2 was upregulated in BC cells with PTX resistance. Loss-of-function studies showed that CTDSPL2 knockdown caused a decrease in cytotoxicity and proliferative ability in PTX-resistant BC cells, as well as enhanced cell apoptotic rate and DNA damage. The results from nanoparticle tracking analysis (NTA) indicated that CTDSPL2 knockdown also suppressed the secretion of extracellular vesicles. In vivo tumorigenesis assays showed that CTDSPL2 downregulation inhibited tumorigenicity of nude mice injecting with PTX-resistant BC cells. Co-immunoprecipitation (Co-IP) assay demonstrated the binding between CTDSPL2 and SCY1-like pseudokinase 1 (SCYL1). The increased level of SCYL1 phosphorylation evoked by CTDSPL2 knockdown in PTX-resistant cancer cells was blocked after mutating the serine 754 site of SCYL1 to alanine. In conclusion, the present study identifies CTDSPL2 as a new factor in BC that plays an essential role in PTX-resistant BC cells through the regulation of SCYL1 phosphorylation.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-18"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13123077/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763433","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}

引用次数: 0

MicroRNAs in chemotherapy-induced peripheral neuropathy: mechanisms and therapies. 化疗诱导的周围神经病变中的microrna：机制和治疗。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2025-12-09 DOI: 10.1080/15384101.2025.2600440

Sepide Javankiani, Faeze Dehghani, Foroozan Yarahmadi, Arian Jahandideh, Fatemeh Asadi, Moein Ghasemi, Danial Akhondi, Zohal Nasiri, Vahid Zarrintan, Mahtab Moradian, Kaveh Mehrvar, Farzad Salmannezhad Khorami, Qumars Behfar

{"title":"MicroRNAs in chemotherapy-induced peripheral neuropathy: mechanisms and therapies.","authors":"Sepide Javankiani, Faeze Dehghani, Foroozan Yarahmadi, Arian Jahandideh, Fatemeh Asadi, Moein Ghasemi, Danial Akhondi, Zohal Nasiri, Vahid Zarrintan, Mahtab Moradian, Kaveh Mehrvar, Farzad Salmannezhad Khorami, Qumars Behfar","doi":"10.1080/15384101.2025.2600440","DOIUrl":"10.1080/15384101.2025.2600440","url":null,"abstract":"Chemotherapy-induced peripheral neuropathy (CIPN) is a significant adverse effect of cancer therapies that profoundly disrupts the quality of life for patients. CIPN is characterized by sensory symptoms such as pain, tingling, and numbness, typically distributed in a \"glove and stocking\" pattern. Its underlying mechanisms remain incompletely understood, involving complex processes such as heightened neuronal excitability, alterations in ion channel function, neuroinflammation, and glial cell activation. MicroRNAs (miRNAs), small non-coding RNA molecules, play a pivotal role in regulating these processes by modulating gene expression and cellular functions. Emerging evidence suggests that specific miRNAs, including miR-30b-5p, miR-155, miR-124, and miR-21, are involved in regulating pathways that contribute to CIPN-related pain. These miRNAs influence the function of ion channels, glial cell activation, and neuroinflammation. MiRNAs hold significant promise as biomarkers for the early detection of CIPN. This review comprehensively examines the current understanding of miRNA-mediated mechanisms contributing to CIPN development. Key miRNAs implicated in modulating these pathways are discussed in detail, including their potential as diagnostic biomarkers and therapeutic targets. By integrating molecular insights with translational approaches, this review provides a framework for future research and clinical applications targeting miRNA pathways to mitigate CIPN and improve outcomes for cancer patients undergoing chemotherapy.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-17"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145707475","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}

引用次数: 0

UBE2C promotes pancreatic cancer progression through PI3K/Akt/mTOR signaling pathway. UBE2C通过PI3K/Akt/mTOR信号通路促进胰腺癌进展。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-05-19 DOI: 10.1080/15384101.2026.2668450

Zhou Zhou, Yuhang Chen, Ping Li

引用次数: 0

BMSCs-derived exosomal miR-196a-5p promotes macrophage M2 polarization and osteogenesis in postmenopausal osteoporosis through regulating Rspo2/Wnt/β-catenin signaling. bmscs来源的外泌体miR-196a-5p通过调节Rspo2/Wnt/β-catenin信号传导促进绝经后骨质疏松症中巨噬细胞M2极化和成骨。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-06-26 DOI: 10.1080/15384101.2026.2691384

Yingwei Zhao, Jingsong Liu, Yubo Zhang, Min Liang, Rui Li, Yansong Wang

{"title":"BMSCs-derived exosomal miR-196a-5p promotes macrophage M2 polarization and osteogenesis in postmenopausal osteoporosis through regulating Rspo2/Wnt/β-catenin signaling.","authors":"Yingwei Zhao, Jingsong Liu, Yubo Zhang, Min Liang, Rui Li, Yansong Wang","doi":"10.1080/15384101.2026.2691384","DOIUrl":"10.1080/15384101.2026.2691384","url":null,"abstract":"This study aimed to investigate the effects of bone marrow mesenchymal stem cell-derived exosomes (BMSCs-EXOs) on postmenopausal osteoporosis (PMOP). Bilateral ovariectomy (OVX) surgery was performed to establish mouse PMOP models. Histological analysis was conducted using hematoxylin and eosin staining. Gene expression was detected using immunohistochemistry and Western blot. miRNA and mRNA were detected using quantitative reverse transcriptase PCR. Cell functions were analyzed using oil red O, alizarin red, and alkaline phosphatase (ALP) staining, and flow cytometry. The interaction between miR-196a-5p and R-spondin 2 (Rspo2) was verified by luciferase and RNA immunoprecipitation assays. We found that BMSCs-EXOs promoted osteogenesis and macrophage M2 polarization. BMSCs-derived exosomal miR-196a-5p enhanced the effects of BMSCs-EXOs on mediating osteogenesis and M2 polarization. Mechanistically, miR-196a-5p targeted Rspo2, activating Wnt/β-Catenin signaling. BMSCs-derived exosomal miR-196a-5p alleviated the effects of M1 macrophages and promoted the osteogenesis of BMSCs, which was reversed by Rspo2. Furthermore, BMSCs-derived exosomal miR-196a-5p promoted the osteogenesis in vivo. However, miR-196a-5p inhibitor exerted the opposite effects, which was reversed by recombinant IL-10. Taken together, BMSCs-derived exosomal miR-196a-5p protects against PMOP by driving macrophage M2 polarization though regulating Rspo2/Wnt/β-Catenin signaling. Therefore, targeting cell-cell communication in the microenvironment of bone lesions may be a promising strategy for PMOP.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-24"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13313200/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148337551","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}

引用次数: 0

Regulatory roles of pyroptosis-associated lncRnas in breast cancer progression and immune microenvironment. 焦热相关lncrna在乳腺癌进展和免疫微环境中的调节作用。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-09-06 DOI: 10.1080/15384101.2026.2726656

Chou-Yi Hsu, Bilal AbdulMajeed Mukhlif, Ozodbek Nematov, Ibrokhim Sapaev, Mirza R Baig, Safa Alkhayyat, Aseel Smerat

{"title":"Regulatory roles of pyroptosis-associated lncRnas in breast cancer progression and immune microenvironment.","authors":"Chou-Yi Hsu, Bilal AbdulMajeed Mukhlif, Ozodbek Nematov, Ibrokhim Sapaev, Mirza R Baig, Safa Alkhayyat, Aseel Smerat","doi":"10.1080/15384101.2026.2726656","DOIUrl":"10.1080/15384101.2026.2726656","url":null,"abstract":"Breast cancer progression and therapeutic response are profoundly influenced by tumor immune interactions, yet the molecular regulators linking cell death pathways with immune modulation remain incompletely understood. Pyroptosis, a gasdermin-mediated inflammatory form of programmed cell death, has emerged as a key determinant of tumor immunity, while long non-coding RNAs are increasingly recognized as critical upstream regulators of cancer signaling. Recent transcriptomic analyses have identified numerous pyroptosis-associated lncRNAs and generated prognostic signatures that stratify patients into distinct risk groups with significantly different survival outcomes. These signatures are closely associated with the tumor immune microenvironment: low-risk tumors exhibit increased infiltration of CD8+ T cells, NK cells, and B cells, together with elevated immune checkpoint expression, whereas high-risk tumors display immunosuppressive features, including M2 macrophage enrichment and higher tumor mutation burden. Mechanistic studies demonstrate that lncRNAs regulate pyroptosis through inflammasome activation, gasdermin-mediated signaling, and epigenetic modulation, thereby influencing tumor growth, metastasis, and therapeutic resistance. Despite these advances, clinical translation remains limited by dependence on retrospective transcriptomic datasets, insufficient mechanistic validation, lack of standardized assays, and scarce prospective clinical evidence. pyroptosis-associated lncRNAs represent a promising link between tumor progression and immune regulation, with considerable potential as prognostic biomarkers and therapeutic targets in breast cancer.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-26"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13556959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896634","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}

引用次数: 0

Upregulation of ITM2A by p53 activation modulates p53 function through physical interaction. p53激活上调ITM2A可通过物理相互作用调节p53功能。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-08-19 DOI: 10.1080/15384101.2026.2717663

Sim Namkoong, Minsu Jang, Jeong In Lee, Siyun Lee, Rackhyun Park, Yangsik Jeong, Eun-Ju Lee, Junsoo Park

{"title":"Upregulation of ITM2A by p53 activation modulates p53 function through physical interaction.","authors":"Sim Namkoong, Minsu Jang, Jeong In Lee, Siyun Lee, Rackhyun Park, Yangsik Jeong, Eun-Ju Lee, Junsoo Park","doi":"10.1080/15384101.2026.2717663","DOIUrl":"10.1080/15384101.2026.2717663","url":null,"abstract":"The tumor suppressor p53 plays a crucial role in preventing cancer development, and its dysfunction is frequently observed in various cancers. This study identifies a novel regulatory interaction between p53 and ITM2A. We found that p53 upregulates ITM2A expression, while ITM2A in turn inhibits p53 function, suggesting a negative feedback loop. ITM2A mRNA levels were reduced across multiple tumor types, particularly in those harboring mutant p53, and low ITM2A expression correlated with poor patient survival. Mechanistically, ITM2A physically interacts with p53, selectively modulates its phosphorylation (reducing Ser392 while enhancing Ser37), and promotes cytoplasmic accumulation of p53. These modifications collectively suppress p53-dependent transcription, an effect consistently observed across multiple cell lines under both basal conditions and upon physiological p53 activation by genotoxic stress. Conversely, ITM2A depletion enhances p53 nuclear accumulation and transcriptional activity. These findings reveal a novel autoregulatory circuit wherein p53 induces ITM2A expression, which then attenuates p53 activity, suggesting ITM2A as a potential prognostic marker and therapeutic target for cancers with dysregulated p53 signaling.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-14"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13501990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788565","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}

引用次数: 0

Citron Kinase, a mitotic kinase with increasing significance in cancer. 香橼激酶，一种在癌症中日益重要的有丝分裂激酶。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-09-13 DOI: 10.1080/15384101.2026.2729549

Elodie Mitri, Caroline Callot, Anastassia Hatzoglou, Arnaud Besson

引用次数: 0