Cell Proliferation最新文献_第6页

Correction to “Targeting RORα in Macrophages to Boost Diabetic Bone Regeneration” 更正“靶向巨噬细胞中的RORα促进糖尿病骨再生”。

IF 5.6 1区生物学

Cell Proliferation Pub Date : 2025-06-20 DOI: 10.1111/cpr.70084

引用次数: 0

Deciphering Age-Dependent ECM Remodelling in Liver: Proteomic Profiling and Its Implications for Aging and Therapeutic Targets 解读肝脏中年龄依赖性ECM重塑：蛋白质组学分析及其对衰老和治疗靶点的影响。

IF 5.6 1区生物学

Cell Proliferation Pub Date : 2025-06-19 DOI: 10.1111/cpr.70087

Juan Liu, Qingru Song, Chen Li, Jiexin Yan, Ni An, Wenzhen Yin, Jinmei Diao, Yuxin Su, Yunfang Wang

{"title":"Deciphering Age-Dependent ECM Remodelling in Liver: Proteomic Profiling and Its Implications for Aging and Therapeutic Targets","authors":"Juan Liu, Qingru Song, Chen Li, Jiexin Yan, Ni An, Wenzhen Yin, Jinmei Diao, Yuxin Su, Yunfang Wang","doi":"10.1111/cpr.70087","DOIUrl":"10.1111/cpr.70087","url":null,"abstract":"Aging is characterised by progressive structural and functional changes in the liver, with the extracellular matrix (ECM) playing a key role in modulating these changes. Our study presents a comprehensive proteomic analysis of the liver ECM across different age stages, uncovering significant age-related changes. Through the identification of 158 ECM proteins in decellularised rat liver scaffolds, we reveal the intricate relationship between ECM composition and liver maturation, as well as the decrease in regenerative capacity. Lumican was identified as a critical regulator with heightened expression in neonatal livers, which is associated with enhanced hepatocyte proliferation and maintenance of stem cell characteristics. Temporal expression analysis distinguished four distinct clusters of ECM proteins, each reflecting the liver's functional evolution from early development to old age. Early developmental stages were marked by proteins essential for liver growth, while adulthood was characterised by a robust ECM supporting metabolic functions. Middle age showed a regulatory shift towards protease balance, and later life was associated with haemostasis-related processes. Our findings underscore the multifaceted role of the ECM in liver health and aging, offering potential opportunities for therapeutic intervention to counteract age-induced liver dysfunction. This study provides a foundational understanding of ECM dynamics in liver aging and sets the stage for the development of innovative strategies to mitigate the effects of age-related liver decline.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 9","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.70087","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

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 5.6 1区生物学

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

{"title":"RETRACTION: CBX8 Interacts with Chromatin PTEN and Is Involved in Regulating Mitotic Progression","authors":"","doi":"10.1111/cpr.70083","DOIUrl":"10.1111/cpr.70083","url":null,"abstract":"\u0000 \u0000 RETRACTION: B. H. Choi, T. M. Colon, E. Lee, Z. Kou, W. Dai, “ CBX8 Interacts with Chromatin PTEN and Is Involved in Regulating Mitotic Progression,” Cell Proliferation 54, no. 11 (2021): e13110. https://doi.org/10.1111/cpr.13110.\u0000 The above article, published online on 15 December 2020 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Deputy Editor, Yunfeng Lin; and John Wiley & Sons Ltd. A third party reported that the PTEN control bands in Figure 1A had previously been published in another article by some of the same authors (Choi et al. 2017 [https://doi.org/10.1186/s40164-017-0079-0]). Author W. Dai responded to an inquiry by the publisher, but the authors were not able to locate the original data for further analysis. The publisher has confirmed that both articles report on different experimental conditions and time points for both sets of PTEN controls. The retraction has been agreed to because the duplication of the PTEN control data from an earlier publication fundamentally compromises the reliability of the reported results. The authors did not respond to our notice regarding the retraction.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 8","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.70083","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

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

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

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

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