Cell Proliferation最新文献_第2页

RETRACTION: CBX8 Interacts with Chromatin PTEN and Is Involved in Regulating Mitotic Progression. 撤回：CBX8与染色质PTEN相互作用并参与调节有丝分裂进程。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-06-19 DOI: 10.1111/cpr.70083

引用次数: 0

Correction to "YTHDF1 Mediates N-Methyl-N-Nitrosourea-Induced Gastric Carcinogenesis by Controlling HSPH1 Translation". 更正“YTHDF1通过控制HSPH1翻译介导n -甲基- n -亚硝基源诱导的胃癌”。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-06-19 DOI: 10.1111/cpr.70076

引用次数: 0

YKT6 Is Essential for Male Fertility by Promoting Meiosis Progression During Spermatogenesis of Mice. 在小鼠精子发生过程中，YKT6通过促进减数分裂进程对雄性生育至关重要。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-06-18 DOI: 10.1111/cpr.70079

Jie Cen, Xiaochen Yu, Ziqi Wang, Wenbo Liu, Jianze Xu, Qian Fang, Fei Gao, Yongzhi Cao, Hongbin Liu

{"title":"YKT6 Is Essential for Male Fertility by Promoting Meiosis Progression During Spermatogenesis of Mice.","authors":"Jie Cen, Xiaochen Yu, Ziqi Wang, Wenbo Liu, Jianze Xu, Qian Fang, Fei Gao, Yongzhi Cao, Hongbin Liu","doi":"10.1111/cpr.70079","DOIUrl":"https://doi.org/10.1111/cpr.70079","url":null,"abstract":"SNARE proteins are required for membrane fusion events throughout the endomembrane system, and are therefore associated with vesicular transport. Here, we found that the SNARE family member, YKT6, is indispensable for male fertility in mice. Conditional Ykt6 knockout in pre-meiotic and meiotic germ cells leads to complete sterility and meiotic arrest in male mice, which exhibit loss of spermatocytes in seminiferous tubules, but without obvious disruption of chromosomal behaviours during meiosis. We observed that the abundance of syncytia increases along with abnormal morphology of the Golgi apparatus, while lysosomes decrease in Ykt6-cKO testes. Quantitative proteomics and immunofluorescent staining both showed dysregulation of vesicular transport in YKT6-deficient spermatocytes. Additionally, the recombinant mouse proteins, HA::YKT6 and MYC::STX1A, could interact in vitro, further supporting a likely role in mediating transport vesicle fusion with the plasma membrane. Finally, the absence of TEX14 signal within syncytia and enlarged TEX14 rings between spermatocytes together suggest a failure to stabilise intercellular bridges in Ykt6-cKO testes. These results demonstrate that YKT6 is required for male fertility by promoting meiosis progression through vesicular transport regulation during spermatogenesis in mice, expanding our understanding of YKT6 functions, and suggesting a possible strategy for future interventions for male infertility in humans.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70079"},"PeriodicalIF":5.9,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tumour Cell Size Control and Its Impact on Tumour Cell Function. 肿瘤细胞大小控制及其对肿瘤细胞功能的影响。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-06-17 DOI: 10.1111/cpr.70080

Min Zhou, Mei Zhou, Yang Jin

{"title":"Tumour Cell Size Control and Its Impact on Tumour Cell Function.","authors":"Min Zhou, Mei Zhou, Yang Jin","doi":"10.1111/cpr.70080","DOIUrl":"https://doi.org/10.1111/cpr.70080","url":null,"abstract":"Cell size is an important component of cell morphological characteristics. It reflects the characteristics of the cell type, nutritional status, growth stage and physiological function. The cell size of cells of the same type tends to be homogeneous and stable. However, in tumour cells, mutations in cell cycle genes and cytoskeletal genes and overexpression of the corresponding signalling pathways often lead to large variations in tumour cell size. Tumour cells regulate cell size and growth and proliferation through multiple signalling pathways, such as PI3K/Akt/mTOR, Myc and Hippo pathways, which work together to regulate cell size and proliferation. This allows tumour cells to adapt to different survival environments. Alterations in cell size also cause tumours to perform different functions, leading to alterations in tumour stemness, invasive migration and anti-tumour immunity by affecting immune cells in the tumour immune microenvironment. In this review, we describe the endogenous and exogenous factors affecting tumour cell size, analyse the mechanisms by which tumour cells regulate cell size and the effects of cell size on tumour malignancy and tumour immunity, summarise the potential therapeutic targets for cell size, and look forward to possible future research directions and clinical applications.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70080"},"PeriodicalIF":5.9,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

FKBP5 Mediates Alveolar Fibroblast Necroptosis During Acute Respiratory Distress Syndrome. FKBP5介导急性呼吸窘迫综合征时肺泡成纤维细胞坏死。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-06-17 DOI: 10.1111/cpr.70075

Dong Zhang, Wei Liu, Ting Sun, Yangyang Xiao, Qiuwen Chen, Xiao Huang, Xiaozhi Wang, Qian Qi, Hao Wang, Tao Wang

{"title":"FKBP5 Mediates Alveolar Fibroblast Necroptosis During Acute Respiratory Distress Syndrome.","authors":"Dong Zhang, Wei Liu, Ting Sun, Yangyang Xiao, Qiuwen Chen, Xiao Huang, Xiaozhi Wang, Qian Qi, Hao Wang, Tao Wang","doi":"10.1111/cpr.70075","DOIUrl":"https://doi.org/10.1111/cpr.70075","url":null,"abstract":"The inflammatory storm is a hallmark of acute respiratory distress syndrome (ARDS), yet effective therapies remain unavailable. FK506-binding protein 51 (FKBP5) has emerged as a regulator of inflammatory responses. In this study, FKBP5 expression was markedly increased in patients with sepsis and correlated with both cytokine levels and disease severity. Using sepsis-induced ARDS models in Fkbp5-/- and bone marrow chimeric mice, this study demonstrated that non-haematopoietic FKBP5 mitigates inflammatory injury. Single-cell transcriptomic analysis identified fibroblasts and epithelial cells as the primary sources of non-haematopoietic FKBP5 in the lung injury. Conditional deletion of FKBP5 in fibroblasts (Col1a2-iCre Fkbp5flox/flox) confirmed the essential role of fibroblast FKBP5 in the inflammatory response during ARDS. Mechanistically, FKBP5-mediated necroptosis of alveolar fibroblasts triggered NF-κB activation, proinflammatory cytokine release, neutrophil recruitment, and the establishment of an inflammatory microenvironment in alveolar epithelial tissue. These findings suggest a potential therapeutic strategy targeting fibroblast FKBP5 and provide a foundation for future clinical investigation in ARDS management.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70075"},"PeriodicalIF":5.9,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

FAM20C Modulates Neuronal Differentiation in Hypoxic-Ischemic Brain Damage via KAP1 Phosphorylation and LINE1 RNA m6A-Dependent H3K9me3 Regulation. FAM20C通过KAP1磷酸化和LINE1 RNA m6a依赖性H3K9me3调控调控缺氧缺血性脑损伤的神经元分化

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-06-13 DOI: 10.1111/cpr.70073

Chen-Xi Feng, Mei Wang, Gen Li, Si-Jia Chu, Di Wu, Xiao-Han Hu, Li-Xiao Xu, Mei Li, Xing Feng

{"title":"FAM20C Modulates Neuronal Differentiation in Hypoxic-Ischemic Brain Damage via KAP1 Phosphorylation and LINE1 RNA m6A-Dependent H3K9me3 Regulation.","authors":"Chen-Xi Feng, Mei Wang, Gen Li, Si-Jia Chu, Di Wu, Xiao-Han Hu, Li-Xiao Xu, Mei Li, Xing Feng","doi":"10.1111/cpr.70073","DOIUrl":"https://doi.org/10.1111/cpr.70073","url":null,"abstract":"Neurodevelopmental impairment due to hypoxic-ischemic brain damage (HIBD) lacks effective biomarkers and therapeutic targets. Based on some cues from published papers, extracellular serine/threonine protein kinase FAM20C was speculated to play a crucial role in the neurodevelopmental impairment of HIBD. In this study, FAM20C was found suppressed in the ischemic hippocampal tissue of HIBD. The inhibition of FAM20C caused by HIBD affected cell differentiation and subsequently caused cognitive impairment. KAP1 was identified as a kinase substrate of FAM20C in the central nervous system. The regulation of the YTHDC1-NCL-KAP1-LINE1 RNA complex by FAM20C was mediated through KAP1 phosphorylation and LINE1 RNA m6A. These alterations consequently modulated the establishment of the H3K9me3 modification on LINE1 DNA, thereby resulting in neuronal differentiation. Furthermore, E2F4, identified as a transcription factor, regulated FAM20C in HIBD. This research has clarified the novel association between FAM20C and HIBD, laying the foundation for innovative diagnostic and therapeutic strategies to counteract neurodevelopmental disruptions arising from neonatal hypoxic-ischemic encephalopathy (HIE).","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70073"},"PeriodicalIF":5.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mechanism of EC-EXOs-Derived THBS3 Targeting CD47 to Regulate BMSCs Differentiation to Ameliorate Bone Loss. ec - exos衍生的THBS3靶向CD47调控骨髓间充质干细胞分化以改善骨质流失的机制

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-06-13 DOI: 10.1111/cpr.70066

Jiaojiao Wang, Zhaokai Zhou, Wenjie Chen, Yun Chen, Qiyue Zheng, Yajun Chen, Zhengxiao Ouyang, Ran Xu, Qiong Lu

{"title":"Mechanism of EC-EXOs-Derived THBS3 Targeting CD47 to Regulate BMSCs Differentiation to Ameliorate Bone Loss.","authors":"Jiaojiao Wang, Zhaokai Zhou, Wenjie Chen, Yun Chen, Qiyue Zheng, Yajun Chen, Zhengxiao Ouyang, Ran Xu, Qiong Lu","doi":"10.1111/cpr.70066","DOIUrl":"https://doi.org/10.1111/cpr.70066","url":null,"abstract":"With the continuous increase of the elderly population and the deepening of population ageing in China, osteoporosis has gradually become one of the significant public health problems. Elucidating the pathophysiological mechanisms that induce osteoporosis and identifying more effective therapeutic targets is of great clinical significance. In this study, in vitro experiments demonstrated that endothelial cell exosomes (EC-EXOs) promoted osteogenic and inhibited adipogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). Aged and ovariectomy (OVX)-induced osteoporosis mice models injected with EC-EXOs confirmed that EC-EXOs delayed bone loss. Proteomic analysis revealed a key protein regulating the differentiation of BMSCs. Expression of THBS3 was significantly higher in EC-EXOs than in Human microvascular endothelial cells (HMEC-1). In vitro and in vivo experiments further validated that THBS3 promoted BMSCs' osteogenic differentiation, inhibited their adipogenic differentiation, and retarded bone loss. Computational biology analysis found that CD47 is a downstream target and potentially functional receptor in BMSCs that bind to THBS3. THBS3 treatment of BMSCs down-regulated the expression of CD47 in in vitro experiments. The aged/OVX models further confirmed that EC-EXOs can regulate the differentiation of BMSCs and delay the process of bone loss via the THBS3-CD47 axis. CD47 antibody may be a potential therapeutic agent for treating ageing-associated bone loss.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70066"},"PeriodicalIF":5.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tryptophan Suppresses FTH1-Driven Ferritinophagy, a Key Correlate of Prognosis in Hepatocellular Carcinoma. 色氨酸抑制fth1驱动的铁蛋白吞噬，是肝细胞癌预后的关键相关因素。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-06-12 DOI: 10.1111/cpr.70074

Xinxiang Cheng, Xin Ge, Chi Zhang, Xingye Yang, Zhengxin Yu, Min Zhang, Wen Cao, Qingtao Ni, Yang Liu, Songbing He, Yin Yuan

{"title":"Tryptophan Suppresses FTH1-Driven Ferritinophagy, a Key Correlate of Prognosis in Hepatocellular Carcinoma.","authors":"Xinxiang Cheng, Xin Ge, Chi Zhang, Xingye Yang, Zhengxin Yu, Min Zhang, Wen Cao, Qingtao Ni, Yang Liu, Songbing He, Yin Yuan","doi":"10.1111/cpr.70074","DOIUrl":"https://doi.org/10.1111/cpr.70074","url":null,"abstract":"Hepatocellular carcinoma (HCC) remains a lethal malignancy with limited therapeutic options. Ferritinophagy, an autophagy-dependent process regulating iron metabolism, has emerged as a key contributor to ferroptosis and tumour progression. This study hypothesised that the ferritinophagy-related gene FTH1 drives HCC pathogenesis by modulating tryptophan metabolism and reactive oxygen species (ROS)-dependent ferroptosis. To test this, we first analysed TCGA data to identify prognostic ferritinophagy genes, revealing FTH1 as a critical risk factor. Functional experiments using FTH1-knockdown/-overexpressing HCC cell lines and xenograft models demonstrated that FTH1 enhances proliferation, migration, and tumour growth by upregulating CYP1A1/CYP1A2 in the tryptophan pathway, thereby increasing the synthesis of 6-hydroxymelatonin (6-HMT). Mechanistically, 6-HMT suppressed ROS and ferroptosis by inhibiting cytochrome P450 oxidoreductase (POR). Concurrently, intracellular tryptophan levels were found to inhibit NCOA4-mediated selective autophagy of FTH1, stabilising FTH1 levels and promoting tumour survival. Collectively, our findings establish FTH1 as a central regulator of ferritinophagy in HCC and reveal its dual role in linking tryptophan metabolism to redox homeostasis. This result provides a hint of how FTH1 influences HCC pathogenesis and positions the tryptophan metabolism pathway as a promising therapeutic target.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70074"},"PeriodicalIF":5.9,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases. 组蛋白去乙酰化酶及其抑制剂在心血管疾病中的作用。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-06-11 DOI: 10.1111/cpr.70077

Li-Ying Zhang, Yue-Yue Wang, Ri Wen, Tie-Ning Zhang, Ni Yang

{"title":"Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.","authors":"Li-Ying Zhang, Yue-Yue Wang, Ri Wen, Tie-Ning Zhang, Ni Yang","doi":"10.1111/cpr.70077","DOIUrl":"https://doi.org/10.1111/cpr.70077","url":null,"abstract":"Histone deacetylase(HDAC) is Zn2+-dependent histone deacetylases that regulate the key signalling pathways involved in gene transcription. 11 isoforms have been identified. Recent in vitro and in vivo studies have shown that HDACs are involved in the pathophysiology of cardiovascular diseases (CVDs) and play important roles in cell proliferation, differentiation and mitochondrial metabolism. In terms of physiological mechanisms, HDAC1-6 may play important roles in normal cardiac development and physiological function, while HDAC7 regulates angiogenesis. In pathological processes, class I HDACs function as pro-hypertrophic mediators, whereas class II HDACs act as anti-hypertrophic mediators. HDAC1-3, 6, 9, and 11 participate in lipid cell formation, oxidative stress and endothelial cell injury through multiple signalling pathways, contributing to the pathogenesis of atherosclerosis. In addition, HDACs also play a role in CVDs such as heart failure, myocardial fibrosis, pulmonary hypertension and diabetic cardiomyopathy. In view of this, we reviewed the regulatory pathways and molecular targets of HDACs in the pathogenesis of CVD. In addition, we summarise the current discovery of inhibitors targeting HDACs. HDAC inhibitors have shown promising therapeutic progress in animal experiments, but clinical trials to demonstrate their efficacy in humans are still lacking. A better understanding of the role of HDACs in CVD provides a new direction for the development of therapeutic interventions and holds significant research value.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70077"},"PeriodicalIF":5.9,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RNF219 RING Finger Domain Mutants Drive Phase Separation to Encapsulate CCR4-NOT and Promote Cell Proliferation. RNF219环指结构域突变驱动相分离包封CCR4-NOT并促进细胞增殖

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-06-11 DOI: 10.1111/cpr.70072

Chen Chen, Chenghao Guo, Ke Fang, Chengqi Lin, Zhuojuan Luo

引用次数: 0