Cell Proliferation最新文献_第2页

YTHDC1 Modulates the Osteogenic Capacity of hPDLSCs via Wnt/β-Catenin Signalling Pathway for the Treatment of Bone Defects in Osteoporosis Rats.

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-03-17 DOI: 10.1111/cpr.70020

Dan Tan, Qilin Li, Zhenzhen Chen, Hongbing Zhang, Pengcheng Rao, Jingxiang Li, Qianke Tao, Jingang Xiao, Jinlin Song

{"title":"YTHDC1 Modulates the Osteogenic Capacity of hPDLSCs via Wnt/β-Catenin Signalling Pathway for the Treatment of Bone Defects in Osteoporosis Rats.","authors":"Dan Tan, Qilin Li, Zhenzhen Chen, Hongbing Zhang, Pengcheng Rao, Jingxiang Li, Qianke Tao, Jingang Xiao, Jinlin Song","doi":"10.1111/cpr.70020","DOIUrl":"https://doi.org/10.1111/cpr.70020","url":null,"abstract":"Human periodontal ligament stem cells (hPDLSCs) have emerged as promising candidates for the treatment of osteoporotic bone defects. Previous studies have indicated that m6A plays a crucial role in regulating the osteogenic differentiation of hPDLSCs. However, research on the relationship between YTHDC1, as a reading protein, and the osteogenic differentiation of hPDLSCs remains unexplored. This study aimed to investigate the biological roles of YTHDC1 in the osteogenic differentiation of hPDLSCs and to explore underlying mechanisms. Dot blot analysis revealed a progressive increase in m6A methylation during osteogenic differentiation, accompanied by significant upregulation of YTHDC1 expression, as evidenced by qPCR and Western blot. Functional assays utilising siRNA-mediated knockdown and lentiviral-mediated overexpression demonstrated that YTHDC1 positively regulated the osteogenic differentiation potential of hPDLSCs. Mechanistically, mRNA-seq analysis implicated the Wnt/β-catenin signalling pathway, which was further validated through rescue experiments with the Wnt inhibitor DKK1. Notably, in vivo experiments showed that hPDLSCs overexpressing YTHDC1 exhibited enhanced bone formation capacity in the osteoporotic rats. In conclusion, our findings suggested that YTHDC1 modulated the osteogenic capacity of hPDLSCs through the Wnt/β-catenin signalling pathway, highlighting its therapeutic potential for treating bone defects in osteoporotic conditions.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70020"},"PeriodicalIF":5.9,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647389","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

Cutting-Edge Advancements in the Antibiotics-Gut Microbiota-Urinary Tumour Axis.

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-03-17 DOI: 10.1111/cpr.70023

Jie Wang, Dengxiong Li, Ruicheng Wu, Dechao Feng

引用次数: 0

Exploring the Single-Cell Dynamics of FOXM1 Under Cell Cycle Perturbations.

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-03-17 DOI: 10.1111/cpr.70019

Tooba Jawwad, Maliwan Kamkaew, Kriengkrai Phongkitkarun, Porncheera Chusorn, Supawan Jamnongsong, Eric W-F Lam, Somponnat Sampattavanich

{"title":"Exploring the Single-Cell Dynamics of FOXM1 Under Cell Cycle Perturbations.","authors":"Tooba Jawwad, Maliwan Kamkaew, Kriengkrai Phongkitkarun, Porncheera Chusorn, Supawan Jamnongsong, Eric W-F Lam, Somponnat Sampattavanich","doi":"10.1111/cpr.70019","DOIUrl":"https://doi.org/10.1111/cpr.70019","url":null,"abstract":"The cell cycle is crucial for maintaining normal cellular functions and preventing replication errors. FOXM1, a key transcription factor, plays a pivotal role in regulating cell cycle progression and is implicated in various physiological and pathological processes, including cancers like liver, prostate, breast, lung and colon cancer. Despite previous research, our understanding of FOXM1 dynamics under different cell cycle perturbations and its connection to heterogeneous cell fate decisions remains limited. In this study, we investigated FOXM1 behaviour in individual cells exposed to various perturbagens. We found that different drugs induce diverse responses due to heterogeneous FOXM1 dynamics at the single-cell level. Single-cell analysis identified six distinct cellular phenotypes: on-time cytokinesis, cytokinesis delay, cell cycle delay, G1 arrest, G2 arrest and cell death, observed across different drug types and doses. Specifically, treatments with PLK1, CDK1, CDK1/2 and Aurora kinase inhibitors revealed varied FOXM1 dynamics leading to heterogeneous cellular outcomes. Our findings affirm that the dynamics of FOXM1 are essential in shaping cellular outcomes, influencing the signals that dictate responses to various stimuli. Our results gave insights into how FOXM1 dynamics contribute to cell cycle fate decisions, especially under different cell cycle perturbations.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70019"},"PeriodicalIF":5.9,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647386","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

Targeting FABP4 to Inhibit AGEs-RAGE/NF-κB Signalling Effectively Ameliorates Nucleus Pulposus Dysfunction and Angiogenesis in Obesity-Related Intervertebral Disc Degeneration.

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-03-16 DOI: 10.1111/cpr.70021

Lin Han, Fudong Li, Huiqiao Wu, Weiheng Wang, Peiwen Chen, Weicheng Xia, Yang Liu, Kaiqiang Sun, Wenbo Lin

{"title":"Targeting FABP4 to Inhibit AGEs-RAGE/NF-κB Signalling Effectively Ameliorates Nucleus Pulposus Dysfunction and Angiogenesis in Obesity-Related Intervertebral Disc Degeneration.","authors":"Lin Han, Fudong Li, Huiqiao Wu, Weiheng Wang, Peiwen Chen, Weicheng Xia, Yang Liu, Kaiqiang Sun, Wenbo Lin","doi":"10.1111/cpr.70021","DOIUrl":"https://doi.org/10.1111/cpr.70021","url":null,"abstract":"Intervertebral disc degeneration (IVDD) is a primary contributor to low back pain, posing significant social and economic burdens. Increasing evidence shows that obesity contributes to IVDD, yet the underlying mechanisms remain elusive. Here, we firstly revealed a causal correlation between obesity and IVDD via a two-sample mendelian randomization analysis and identified fatty acid-binding protein 4 (FABP4) as the potential regulator to associate IVDD and obesity. Elevated FABP4 expression promoted extracellular matrix (ECM) disequilibrium and angiogenesis to exacerbate IVDD progression. Genetically knocking out or pharmacologically inhibiting FABP4 in high-fat diet-induced mice alleviated IVDD. Mechanistically, obesity activated the mammalian target of rapamycin complex 1 (mTORC1), which upregulated FABP4 expression, leading to the accumulation of advanced glycation end-products (AGEs) in intervertebral disc tissue. AGEs further activated the NF-κB signalling pathway, exacerbating ECM degradation and neovascularization. Conversely, rapamycin-mediated inhibition of mTORC1 suppressed FABP4 expression in nucleus pulposus cells (NPCs), alleviating IVDD in vivo. Collectively, our findings reveal a critical role of the obesity-induced mTORC1-FABP4 axis in ECM degradation and angiogenesis during IVDD progression. Targeting FABP4 may represent a promising therapeutic strategy for IVDD in obese individuals.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70021"},"PeriodicalIF":5.9,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143639566","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 Metabolic Enzyme IL4I1 Inhibits Ferroptosis by Decreasing Ubiquitination of Nrf2 via I3P in Glioblastoma.

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-03-12 DOI: 10.1111/cpr.13816

Yang Xu, Yu Hong, Tengfeng Yan, Qian Sun, Fanen Yuan, Shanwen Liang, Liguo Ye, Rongxin Geng, Yangzhi Qi, Qingsong Ye, Qianxue Chen

{"title":"Tryptophan Metabolic Enzyme IL4I1 Inhibits Ferroptosis by Decreasing Ubiquitination of Nrf2 via I3P in Glioblastoma.","authors":"Yang Xu, Yu Hong, Tengfeng Yan, Qian Sun, Fanen Yuan, Shanwen Liang, Liguo Ye, Rongxin Geng, Yangzhi Qi, Qingsong Ye, Qianxue Chen","doi":"10.1111/cpr.13816","DOIUrl":"https://doi.org/10.1111/cpr.13816","url":null,"abstract":"Glioblastoma multiforme (GBM) is the deadliest brain tumour with an extremely poor prognosis. Tryptophan catabolism could enhance an array of protumour-genic signals and promoted tumour progression in GBM. However, the mechanisms of oncogenic signalling under tryptophan catabolism and potential therapy targeting this pathway have not been completely understood. Interleukin 4-induced 1 (IL4I1) is newly defined as a tryptophan metabolic enzyme and the potential function in GBM cells still remains unclear. In our study, we found IL4I1 was upregulated in GBM patients and predicted poor prognosis. Upregulation of IL4I1 inhibited GBM ferroptosis in vitro and in vivo. Further, we found that indole-3-pyruvic acid (I3P) from tryptophan mediated by IL4I1 could scavenge free radical and had an impressive role in inhibiting ferroptosis. To clarify the potential mechanism of I3P in GBM ferroptosis, we performed transcriptomic analyses of GBM cells treated with I3P and found that Nrf2 related genes was upregulated. Further, we found that the ubiquitination of Nrf2 could be attenuate by I3P binding with Nrf2 directly. Knockdown of Nrf2 attenuated the induction of anti-ferroptosis by IL4I1, pointing to Nrf2 as a key mediator of this process. In vivo, overexpression of IL4I1 with ML385 in GBM xenografts promoted ferroptosis. Collectively, this study emphasises the crucial roles of IL4I1 in anti-ferroptosis through Nrf2 signalling pathway but not AHR pathway by catabolism tryptophan, suggesting IL4I1 and tryptophan reprogramming as potential therapeutic targets for GBM.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13816"},"PeriodicalIF":5.9,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604146","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

Sirt3 Rescues Porphyromonas gingivalis-Impaired Cementogenesis via SOD2 Deacetylation.

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-03-11 DOI: 10.1111/cpr.70022

Xin Huang, Huiqing Gou, Jirong Xie, Yonglin Guo, Yifei Deng, Yan Xu, Zhengguo Cao

{"title":"Sirt3 Rescues Porphyromonas gingivalis-Impaired Cementogenesis via SOD2 Deacetylation.","authors":"Xin Huang, Huiqing Gou, Jirong Xie, Yonglin Guo, Yifei Deng, Yan Xu, Zhengguo Cao","doi":"10.1111/cpr.70022","DOIUrl":"https://doi.org/10.1111/cpr.70022","url":null,"abstract":"The keystone pathogen Porphyromonas gingivalis (P.g.) is responsible for cementum resorption in periodontitis; however, the mechanism involved in it remains unclear. Sirtuin 3 (Sirt3) is a NAD+-dependent protein deacetylase contributing to mitochondrial homeostasis and various cell functions. In this study, the expression of Sirt3 in cementoblasts was found to be increased during cementoblast mineralisation and cementum development, while it decreased gradually under P.g. infection in a multiplicity of infection-dependent manner. Compared with wild type mice, the Sirt3 knockout mice showed less cellular cementum and lower mineralisation capacity with decreased expression of Runx2 and OCN in cementoblasts. Sirt3 inhibition by 3-TYP or Sirt3 silencing by lentivirus infection both confirmed the impaired cementogenesis. Conversely, honokiol (HKL) was simulated to bind Sirt3 and was applied to activate Sirt3 in cementoblasts. HKL-mediated Sirt3 activation facilitated cementoblast mineralisation and rescued P.g.-suppressed cementoblast mineralisation markedly. Superoxide dismutase 2 (SOD2), the downstream molecule of Sirt3, showed a similar expression pattern to Sirt3 under different conditions. Silencing of SOD2 was demonstrated to restrain cementoblast mineralisation. The pan acetylation was detected to decrease under Sirt3-upregulating conditions and increase under Sirt3-downregulating conditions. The binding of Sirt3 and SOD2 in cementoblasts was also verified. Furthermore, SOD2 acetylation and specific SOD2-K68 acetylation were found to be upregulated under P.g. or Sirt3 silencing conditions and downregulated by HKL stimulation. Moreover, K68Q mutation simulating acetylation decreased cementoblast mineralisation, while K68R mutation simulating deacetylation increased it. Altogether, Sirt3 deacetylates SOD2 via K68 to orchestrate P.g.-perturbed cementogenesis, and HKL is a Sirt3-targeted treatment candidate.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70022"},"PeriodicalIF":5.9,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604192","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

Rapid and Effective Neuronal Conversion of Human Glioblastoma In Vitro and In Vivo Using Potent Small Molecules.

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-03-11 DOI: 10.1111/cpr.70013

Ya'nan Hu, Jinming Liu, Jian Tu, Min Yang, Qisheng He, Fei Li, Xiaojing Xu, Zhongqing Ji, Jianwei Xu, Wentao Zhong, Mengwen Yan, Ying Yang, Huanxiang Zhang

{"title":"Rapid and Effective Neuronal Conversion of Human Glioblastoma In Vitro and In Vivo Using Potent Small Molecules.","authors":"Ya'nan Hu, Jinming Liu, Jian Tu, Min Yang, Qisheng He, Fei Li, Xiaojing Xu, Zhongqing Ji, Jianwei Xu, Wentao Zhong, Mengwen Yan, Ying Yang, Huanxiang Zhang","doi":"10.1111/cpr.70013","DOIUrl":"https://doi.org/10.1111/cpr.70013","url":null,"abstract":"Exploring effective, prompt and universally applicable approaches for inducing the differentiation of glioblastoma (GBM) into terminally differentiated cells, such as astrocytes or neurons that cease cell division, is pivotal for the success of GBM differentiation therapy. In this study, a neuronal-specific promoter-reporter system was employed to screen small molecules that promote neural differentiation. The cocktail YFSS, consisting of Y27632, Forskolin, SB431542 and SP600125, which selectively targets the ROCK, cAMP, TGF-β and JNK signalling pathways, respectively, was found to effectively trigger differentiation in human GBM cells. This process yielded neuron-like cells within 7 days, inhibited GBM cell proliferation and reduced malignancy traits, such as stemness, migratory and invasive capabilities. Transcriptome sequencing revealed the pathways altered by YFSS, shedding light on its dual role in halting cell proliferation and initiating neuronal differentiation. A notable increase in CEND1 expression, a key molecule in cell cycle and neuronal differentiation regulation, was observed during differentiation. However, CEND1 alone could not replicate YFSS's high conversion efficiency and its depletion reduced the differentiation and restored proliferation of the GBM cells. In vivo, prolonged and localised YFSS application significantly curtailed tumour growth and extended survival in patient-derived xenograft mice models. In summary, our findings reveal that the small-molecule cocktail YFSS is an effective means for inducing neuronal differentiation in GBM cells, representing a novel and promising pathway for the advancement of GBM treatment.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70013"},"PeriodicalIF":5.9,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604187","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

Targeting Regulation of Macrophage to Treat Metabolic Disease: Role of Phytochemicals.

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-03-05 DOI: 10.1111/cpr.70012

Zeting Ye, Yanlin Li, Xiaolin Yang, Chenglin Li, Rui Yu, Guangjuan Zheng, Zuqing Su

{"title":"Targeting Regulation of Macrophage to Treat Metabolic Disease: Role of Phytochemicals.","authors":"Zeting Ye, Yanlin Li, Xiaolin Yang, Chenglin Li, Rui Yu, Guangjuan Zheng, Zuqing Su","doi":"10.1111/cpr.70012","DOIUrl":"https://doi.org/10.1111/cpr.70012","url":null,"abstract":"Metabolic syndrome encompasses a cluster of predictive metabolic risk factors, including obesity, insulin resistance, dyslipidemia, hyperglycemia and hypertension. It is strongly associated with the development of type 2 diabetes and cardiovascular disease. Given the increasing morbidity and mortality associated with metabolic syndrome, along with the limited availability of drug treatments, it is high time to investigate the pathogenesis of this condition and explore potential pharmacotherapies. Macrophages, well-known innate immune cells, play an essential role in maintaining tissue immune homeostasis and multiple physiological processes, including glucose and lipid metabolism, oxidative stress and inflammation. Emerging evidence indicates that the effects of macrophages in metabolic syndrome are linked to macrophage-mediated metaflammation. Phytochemicals derived from natural plants have been shown to exert therapeutic effects on metabolic syndrome by modulating macrophage function. In this review, we sort out the role of macrophage-mediated metaflammation in the pathogenesis of metabolic syndrome and summarise potential phytochemicals that target macrophages for the treatment of this condition.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70012"},"PeriodicalIF":5.9,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566249","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

Featured Cover

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-03-05 DOI: 10.1111/cpr.13822

Lanyang Gao, Lin Gao, Shiyao Huang, Lei Sun, Mei Li, Chen Shen, Youyou Chen, Ruihao Tan, Yuji Chen, Chengguo Zhan, Frank Heinrich Wieland, Yingying Liu, Yinan Zhang, Yao Luo

引用次数: 0

Multi-Omics Reveal the Metabolic Changes in Cumulus Cells During Aging.

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-03-05 DOI: 10.1111/cpr.70014

Liangyue Shi, Hengjie Wang, Shuai Zhu, Minjian Chen, Xuejiang Guo, Qiang Wang, Ling Gu

{"title":"Multi-Omics Reveal the Metabolic Changes in Cumulus Cells During Aging.","authors":"Liangyue Shi, Hengjie Wang, Shuai Zhu, Minjian Chen, Xuejiang Guo, Qiang Wang, Ling Gu","doi":"10.1111/cpr.70014","DOIUrl":"https://doi.org/10.1111/cpr.70014","url":null,"abstract":"Maternal age has been reported to impair oocyte quality. However, the molecular mechanisms underlying the age-related decrease in oocyte competence remain poorly understood. Cumulus cells establish direct contact with the oocyte through gap junctions, facilitating the provision of crucial nutrients necessary for oocyte development. In this study, we obtained the proteomic and metabolomic profiles of cumulus cells from both young and old mice. We found that fatty acid beta-oxidation and nucleotide metabolism, markedly active in aged cumulus cells, may serve as a compensatory mechanism for energy provision. Tryptophan undergoes two principal metabolic pathways, including the serotonin (5-HT) synthesis and kynurenine catabolism. Notably, we discovered that kynurenine catabolism is reduced in aged cumulus cells compared to young cells, whereas 5-HT synthesis exhibited a significant decrease. Furthermore, the supplement of 5-HT during cumulus-oocyte complexes (COCs) culture significantly ameliorated the metabolic dysfunction and meiotic defects in old oocytes. In sum, our data provide a comprehensive multiple omics resource, offering potential insights for improving oocyte quality and promoting fertility in aged females.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70014"},"PeriodicalIF":5.9,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566237","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