Cell Proliferation最新文献_第3页

Autophagy in PE: Dispute, Role and Potential Target. PE中的自噬：争议、作用和潜在目标。

IF 5.6 1区生物学

Cell Proliferation Pub Date : 2025-08-12 DOI: 10.1111/cpr.70102

Miao Xu, Qi Wang, Fang Wang, Li Kang, Huijing Ma, Mengnan Li, Zhuanghui Hao, Zhengrui Li, Ji'an Liu, Xufeng Huang, Hengrui Liu, Shouxin Wei, Hailan Yang

引用次数: 0

Featured Cover 了封面

IF 5.6 1区生物学

Cell Proliferation Pub Date : 2025-08-11 DOI: 10.1111/cpr.70106

Tingting Wu, Weihao Li, Liujing Zhuang, Jinxia Liu, Ping Wang, Ye Gu, Yongliang Liu, Yiqun Yu

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Piezo2 in Mechanosensory Biology: From Physiological Homeostasis to Disease-Promoting Mechanisms. 机械感觉生物学中的Piezo2：从生理稳态到疾病促进机制。

IF 5.6 1区生物学

Cell Proliferation Pub Date : 2025-08-09 DOI: 10.1111/cpr.70112

Zhebin Cheng, Zuping Wu, Mengjie Wu, Liang Xie, Qianming Chen

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Pioglitazone Ameliorates Mitochondrial Oxidative Stress and Inflammation via AMPK-Dependent Inhibition of Mitochondrial Fission in Leigh Syndrome. 吡格列酮通过ampk依赖性抑制Leigh综合征线粒体裂变改善线粒体氧化应激和炎症。

IF 5.6 1区生物学

Cell Proliferation Pub Date : 2025-08-06 DOI: 10.1111/cpr.70109

Jie Luo, Ling Chen, Xiaoxian Zhang, Qiang Su, Xiaoya Zhou, Qizhou Lian

{"title":"Pioglitazone Ameliorates Mitochondrial Oxidative Stress and Inflammation via AMPK-Dependent Inhibition of Mitochondrial Fission in Leigh Syndrome.","authors":"Jie Luo, Ling Chen, Xiaoxian Zhang, Qiang Su, Xiaoya Zhou, Qizhou Lian","doi":"10.1111/cpr.70109","DOIUrl":"https://doi.org/10.1111/cpr.70109","url":null,"abstract":"Loss of function mutations of NDUFS4 resulted in Leigh syndrome, which is a progressive neurodegenerative disease and characterized by mitochondrial oxidative stress, inflammation and aberrant mitochondrial dynamics. However, there is currently no effective treatment. Here, we demonstrate that pioglitazone significantly mitigates mitochondrial reactive oxygen species (ROS) generation, lowers cyclooxygenase-2 (COX-2) mRNA levels, and rescues aberrant mitochondrial dynamics in vitro (increasing Opa-1 expression while decreasing Drp-1 expression). Furthermore, similar effects were observed with the selective Drp-1 inhibitor mdivi-1, suggesting that inhibiting mitochondrial fission mediates the therapeutic effects of pioglitazone. Pioglitazone administration activated AMPK phosphorylation, but these effects, along with pioglitazone's ability to reverse oxidative stress, inflammation, and mitochondrial fission, were abolished by the AMPK inhibitor compound C. In vivo, pioglitazone alleviated motor dysfunction, prolonged lifespan, and promoted weight gain in Ndufs4 KO mice. This was accompanied by enhanced mitochondrial fusion and increased levels of mitochondrial complex subunits. Consistently, pioglitazone attenuated neuroinflammation and oxidative stress in vivo. Collectively, our findings indicate that pioglitazone alleviates mitochondrial oxidative stress and inflammation through an AMPK-dependent inhibition of Drp-1-mediated mitochondrial fission. Therefore, suppression of mitochondrial fission may represent a novel therapeutic strategy for Leigh syndrome (LS).","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70109"},"PeriodicalIF":5.6,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788377","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

Correction to “Circadian BMAL1 Regulates Mandibular Condyle Development by Hedgehog Pathway” 更正“昼夜节律BMAL1通过刺猬通路调节下颌髁发育”。

IF 5.6 1区生物学

Cell Proliferation Pub Date : 2025-08-05 DOI: 10.1111/cpr.70111

引用次数: 0

Transcription Factor TCF12-Mediated Maternal Gene Expressions in Mouse Oocyte Are Prerequisites of Successful Fertilisation and Zygotic Genome Activation. 转录因子tcf12介导的母基因在小鼠卵母细胞中的表达是成功受精和合子基因组激活的先决条件。

IF 5.6 1区生物学

Cell Proliferation Pub Date : 2025-08-03 DOI: 10.1111/cpr.70110

Lan-Rui Cao, Chi Zhang, Zuo-Qi Deng, Yue-Xin Qiu, Zhao Zhang, Heng-Yu Fan, Jing Li, Hong-Bo Wu

{"title":"Transcription Factor TCF12-Mediated Maternal Gene Expressions in Mouse Oocyte Are Prerequisites of Successful Fertilisation and Zygotic Genome Activation.","authors":"Lan-Rui Cao, Chi Zhang, Zuo-Qi Deng, Yue-Xin Qiu, Zhao Zhang, Heng-Yu Fan, Jing Li, Hong-Bo Wu","doi":"10.1111/cpr.70110","DOIUrl":"https://doi.org/10.1111/cpr.70110","url":null,"abstract":"The maternal gene products stored in oocytes control the initial development of multicellular animals. Alteration within the dual allelic variants of transcription factor TCF12 causes female infertility; however, its impact on female reproduction is still unknown. In this study, we provide evidence that TCF12 is abundantly expressed within the nucleus of oocytes during growth at the germinal vesicle (GV) stage, recognising and binding to the functional domain of target genes to moderate transcriptional activity. The absence of Tcf12 in oocytes during the primordial follicular phase causes female sterility. Tcf12 does not participate in meiotic maturation; however, unlike Tcf3, it is essential for fertilisation and preimplantation development. Tcf12 maintains fertilisation competence by controlling the proper expression and location of cortical granules and protease ovastacin (encoded by Astl). In contrast, zygotes without TCF12 have a prolonged mitotic cell cycle upon a decrease in protein phosphatase 2A (PP2A) activity inhibition, resulting in zygotic genome activation (ZGA) failure during the 2-cell stage. Maternal knockout embryos gradually lose their developmental potential in subsequent developmental processes. These observations indicate that the maternal effect induced by Tcf12 ensures preimplantation development.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70110"},"PeriodicalIF":5.6,"publicationDate":"2025-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774746","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

Dysregulation of Rho-Associated Coiled-Coil Protein Kinase1 Depletes Neural Stem Cell Pool and Impairs Hippocampal Neurogenesis After Traumatic Brain Injury. 创伤性脑损伤后rho相关卷曲蛋白激酶1的失调消耗神经干细胞库并损害海马神经发生

IF 5.6 1区生物学

Cell Proliferation Pub Date : 2025-08-01 DOI: 10.1111/cpr.70093

Chaoqun Yao, Long Jin, Jun Zhong, Qianying Huang, Zhongwei Bao, Shaolong Zhou, Chaohua Wang, Huanhuan Li, Xiaowei Yuan, Zhen Wang, Ning Du, Jingxuan Yu, Huanran Chen, Xuyang Zhang, Hongfei Ge, Jianheng Wu

{"title":"Dysregulation of Rho-Associated Coiled-Coil Protein Kinase1 Depletes Neural Stem Cell Pool and Impairs Hippocampal Neurogenesis After Traumatic Brain Injury.","authors":"Chaoqun Yao, Long Jin, Jun Zhong, Qianying Huang, Zhongwei Bao, Shaolong Zhou, Chaohua Wang, Huanhuan Li, Xiaowei Yuan, Zhen Wang, Ning Du, Jingxuan Yu, Huanran Chen, Xuyang Zhang, Hongfei Ge, Jianheng Wu","doi":"10.1111/cpr.70093","DOIUrl":"https://doi.org/10.1111/cpr.70093","url":null,"abstract":"Traumatic brain injury (TBI) represents a global health burden, often resulting in persistent neurological deficits due to impaired hippocampal neurogenesis. Nevertheless, the temporal progression of post-TBI neurogenesis and its molecular mechanisms remain elusive. To investigate the mechanism of impaired hippocampal neurogenesis and neurological deficits following TBI. Single-cell RNA sequencing (scRNA-seq) was employed to explore the mechanism of abnormal hippocampal neurogenesis after TBI in mice. Antagonists and conditional gene knockout (CKO) strategies were applied to dissect the molecular function of target genes. Here, we found that neural stem cells (NSCs) were hyperactivated as observed in Nestin-GFP reporter mice in hippocampus during the early phases of TBI, followed by progressive depletion of the NSC pool, impaired neurogenesis, and the onset of progressive cognitive dysfunction. ScRNA-seq transcriptomic analysis revealed sustained upregulation of Rho-associated coiled-coil protein kinase 1 (ROCK1) in hippocampal NSCs post-TBI. Pharmacological inhibition of ROCK1 or ROCK1 CKO rescued chronic neurogenic deficits and improved cognitive functions in TBI mice. Mechanistically, ROCK1 dysregulation impaired neurogenesis via aberrant AKT hyperphosphorylation, establishing a unidirectional ROCK1-AKT signalling axis in adult hippocampal neurogenesis. Our findings position ROCK1 as a pivotal regulator of the post-TBI NSC pool hyperactivation and aberrant neurogenesis and propose targeted kinase inhibition strategies as a potential therapy to mitigate abnormal neurogenesis in TBI patients.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70093"},"PeriodicalIF":5.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764608","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

PIK-III-Mediated Elevation of Thiamine Re-Sensitises Renal Cell Carcinoma to Cuproptosis via Activating PDHA1. pik - iii通过激活PDHA1介导的硫胺素对肾细胞癌铜增生再敏感的升高。

IF 5.6 1区生物学

Cell Proliferation Pub Date : 2025-07-31 DOI: 10.1111/cpr.70101

Dongdong Xie, Yu Wang, Wenjie Cheng, Minbo Yan, Kunyu Li, Xiang Wu, Jiaqing Wu, Zhuangzhuang Zhang, Yingbo Dai

{"title":"PIK-III-Mediated Elevation of Thiamine Re-Sensitises Renal Cell Carcinoma to Cuproptosis via Activating PDHA1.","authors":"Dongdong Xie, Yu Wang, Wenjie Cheng, Minbo Yan, Kunyu Li, Xiang Wu, Jiaqing Wu, Zhuangzhuang Zhang, Yingbo Dai","doi":"10.1111/cpr.70101","DOIUrl":"https://doi.org/10.1111/cpr.70101","url":null,"abstract":"Cuproptosis, a copper-dependent cell death mechanism driven by tricarboxylic acid (TCA) cycle collapse, shows limited efficacy in hypoxic or glycolytic renal cell carcinoma (RCC). Here, through systematic screening of 688 glycolysis inhibitors combined with elesclomol (ES), we identified PIK-III as a potent cuproptosis sensitiser. Multi-omics analysis revealed that PIK-III restores sensitivity by rewiring thiamine metabolism. Mechanistically, PIK-III induces macropinocytosis, enabling thiamine uptake to replenish thiamine pyrophosphate (TPP), which activates pyruvate dehydrogenase E1-alpha 1 (PDHA1) and redirects pyruvate into the TCA cycle. Concurrently, ES-induced DLAT oligomerisation disrupts TCA flux, creating a metabolic crisis. In vivo, PIK-III synergises with ES to suppress tumour growth in xenograft and patient-derived models without systemic toxicity. Our work uncovers a metabolic vulnerability in cuproptosis-resistant RCC and positions PIK-III as a therapeutic candidate to overcome resistance via dual targeting of thiamine transport and mitochondrial dysfunction.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70101"},"PeriodicalIF":5.6,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752530","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

PTRF Confers Melanoma-Acquired Drug Resistance Through the Upregulation of EGFR. PTRF通过上调EGFR使黑色素瘤获得性耐药。

IF 5.6 1区生物学

Cell Proliferation Pub Date : 2025-07-31 DOI: 10.1111/cpr.70086

Miao Wang, Ying Cao, Chengcheng Ren, Ke Wang, Yaxiang Wang, Xiaoying Wu, Jian Mao, Qian Liang, Qian Zhang, Hezhe Lu, Xiaowei Xu, Yu-Sheng Cong

{"title":"PTRF Confers Melanoma-Acquired Drug Resistance Through the Upregulation of EGFR.","authors":"Miao Wang, Ying Cao, Chengcheng Ren, Ke Wang, Yaxiang Wang, Xiaoying Wu, Jian Mao, Qian Liang, Qian Zhang, Hezhe Lu, Xiaowei Xu, Yu-Sheng Cong","doi":"10.1111/cpr.70086","DOIUrl":"https://doi.org/10.1111/cpr.70086","url":null,"abstract":"Melanoma is the most serious type of skin cancer. About half of all melanomas have activating BRAF mutations. Targeted therapy for malignant melanoma with BRAF inhibitor (BRAFi) or its combination with MEK inhibitor (MEKi) improves the clinical outcomes of patients, but resistance develops invariably. The underlying mechanisms remain incompletely understood. Here, we show that caveolae number is increased in both BRAFi and BRAFi + MEKi-resistant melanoma cells, and the expression of the critical caveolae component PTRF is significantly upregulated in drug-resistant melanoma cell lines and tumour tissues. Knockdown of PTRF in drug-resistant cells reduces proliferation with increased apoptosis, whereas ectopic expression of PTRF confers resistance on parental cells to BRAFi or BRAFi + MEKi. On the contrary, the knockdown of PTRF in parental cells reduces their ability to acquire drug resistance induced by BRAFi treatment. Interestingly, we find that the expression of EGFR is increased along with PTRF and caveolin-1 in drug-resistant cells and in PTRF transduced parental cells, whereas knockdown of PTRF results in down-regulation of EGFR expression and attenuates drug resistance of parental cells induced by PTRF expression. Together, these results suggest that PTRF contributes to therapy resistance through upregulating EGFR in melanoma cells.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70086"},"PeriodicalIF":5.6,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759220","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

Kdf1 Regulates Molar Cusp Morphogenesis via the PI3K/AKT/mTOR Signalling Axis. Kdf1通过PI3K/AKT/mTOR信号轴调控臼齿尖的形态发生。

IF 5.6 1区生物学

Cell Proliferation Pub Date : 2025-07-30 DOI: 10.1111/cpr.70108

Jiayu Wang, Miao Yu, Hangbo Liu, Kai Sun, Chenxin Geng, Haochen Liu, Hailan Feng, Yang Liu, Hu Zhao, Dong Han

{"title":"Kdf1 Regulates Molar Cusp Morphogenesis via the PI3K/AKT/mTOR Signalling Axis.","authors":"Jiayu Wang, Miao Yu, Hangbo Liu, Kai Sun, Chenxin Geng, Haochen Liu, Hailan Feng, Yang Liu, Hu Zhao, Dong Han","doi":"10.1111/cpr.70108","DOIUrl":"https://doi.org/10.1111/cpr.70108","url":null,"abstract":"Keratinocyte differentiation factor 1 (Kdf1) reportedly plays a significant role in enamel formation. In terms of tooth morphogenesis, human KDF1 variants are associated with crown morphological abnormalities, suggesting that Kdf1 may also be essential for tooth morphogenesis. However, the involvement of Kdf1 in tooth morphogenesis and its underlying mechanisms remains unclear. In this study, we observed that mice lacking epithelial Kdf1 (K14-Cre;Kdf1fl/fl) displayed rounded and blunt molar cusps, resembling the morphological anomalies observed in patients with Kdf1 variants. 5-Ethynyl-2'-deoxyuridine assays revealed increased proliferative activity of the inner enamel epithelial (IEE) cells in the cusp region of K14-Cre;Kdf1fl/fl mice during the bell stage. RNA sequencing and western blot analysis confirmed the overactivation of PI3K/AKT/mTOR signalling in the molar IEE cells of K14-Cre;Kdf1fl/fl mice. Furthermore, in utero microcapillary injection of the PI3K/AKT/mTOR pathway inhibitor LY294002 partially rescued the molar cusp defects in K14-Cre;Kdf1fl/fl mice. Collectively, our findings provide in vivo evidence supporting the regulatory role of Kdf1 in molar cusp morphogenesis, highlighting its function in modulating dental epithelial cell proliferation via the PI3K/AKT/mTOR signalling pathway.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70108"},"PeriodicalIF":5.6,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752529","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