Cell Cycle最新文献_第2页

α-Fodrin-CENP-E interaction is critical for pancreatic cancer progression and drug response. α-Fodrin-CENP-E相互作用对胰腺癌进展和药物反应至关重要。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-04-10 DOI: 10.1080/15384101.2025.2485837

Athira Jyothy, Julfequar Hussain, Sharanya C S, Vineetha Radhakrishnan Chandraprabha, Madhumathy G Nair, Smreti Vasudevan, Hariharan Sreedharan, Betty Abraham, Tessy Thomas Maliekal, Kathiresan Natarajan, Suparna Sengupta

{"title":"α-Fodrin-CENP-E interaction is critical for pancreatic cancer progression and drug response.","authors":"Athira Jyothy, Julfequar Hussain, Sharanya C S, Vineetha Radhakrishnan Chandraprabha, Madhumathy G Nair, Smreti Vasudevan, Hariharan Sreedharan, Betty Abraham, Tessy Thomas Maliekal, Kathiresan Natarajan, Suparna Sengupta","doi":"10.1080/15384101.2025.2485837","DOIUrl":"https://doi.org/10.1080/15384101.2025.2485837","url":null,"abstract":"α-Fodrin, a known scaffolding protein for cytoskeleton stabilization, performs various functions including cell adhesion, cell motility, DNA repair and apoptosis. Based on our previous results revealing its role in mitosis in glioblastoma, we have examined its effect in pancreatic cancer, which is often linked to mitotic aberrations including aneuploidy and chromosome instability. Here, we show that the expression of α-Fodrin increases in pancreatic adenocarcinoma tissues compared to its normal counterpart, suggesting its tumor promoting role. shRNA-mediated knock-down of α-Fodrin significantly reduces the xenograft growth in immunocompromised mice underscoring the importance of α-Fodrin in tumor progression. CENP-E (centromere-associated protein E) is a motor protein essential for chromosomal alignment and segregation during mitosis. We have found that α-Fodrin interacts with CENP-E to recruit it to the kinetochore and depletion of α-Fodrin has a crucial role in controlling aneuploidy. As these mitotic defects can lead to apoptosis, we have further evaluated the activation of possible upstream pathways. Paclitaxel, a chemotherapeutic agent that stabilizes microtubules, disrupts mitosis and induces apoptosis. We found that Paclitaxel triggered stronger activation of JNK, ERK, and P38 MAPKs, altered BCL2/BAX ratios, cytochrome C release causing increased apoptosis in α-Fodrin knockdown cells compared to cells with wild-type α-Fodrin. This enhanced sensitivity to paclitaxel is consistent with improved survival in pancreatic cancer patients with low α-Fodrin (SPTAN1) and low CENP-E expression compared to poor prognosis with high expressions of both the genes. Taken together, this study provides the molecular mechanism by which α-Fodrin - CENP-E axis regulates pancreatic cancer progression and drug response.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-25"},"PeriodicalIF":3.4,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143954791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

High GLP1R gene copy numbers associated with microsatellite instability for multiple cancers and with better survival probabilities for glioblastoma. 高GLP1R基因拷贝数与多种癌症的微卫星不稳定性和胶质母细胞瘤的更好生存概率相关。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-04-10 DOI: 10.1080/15384101.2025.2485873

Teresa M Thomas, Michael T Aboujaoude, Vayda R Barker, Mallika Varkhedi, Rahul Jain, George Blanck

引用次数: 0

Leaving the mark: FMOs as an emerging class of cytokinetic regulators. 留下印记：FMOs作为一种新兴的细胞动力学调节剂。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-04-08 DOI: 10.1080/15384101.2025.2485843

Léa Lacroix, Eugénie Goupil, Matthew J Smith, Jean-Claude Labbé

引用次数: 0

Exosomes derived from mesenchymal stem cells ameliorate impaired glucose metabolism in myocardial Ischemia/reperfusion injury through miR-132-3p/PTEN/AKT pathway. 来自间充质干细胞的外泌体通过miR-132-3p/PTEN/AKT通路改善心肌缺血/再灌注损伤中的糖代谢受损。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-04-03 DOI: 10.1080/15384101.2025.2485834

Hongkun Wu, Yongpeng Hui, Xingkai Qian, Xueting Wang, Jianwei Xu, Feng Wang, Sisi Pan, Kaiyuan Chen, Zhou Liu, Weilong Gao, Jue Bai, Guiyou Liang

{"title":"Exosomes derived from mesenchymal stem cells ameliorate impaired glucose metabolism in myocardial Ischemia/reperfusion injury through miR-132-3p/PTEN/AKT pathway.","authors":"Hongkun Wu, Yongpeng Hui, Xingkai Qian, Xueting Wang, Jianwei Xu, Feng Wang, Sisi Pan, Kaiyuan Chen, Zhou Liu, Weilong Gao, Jue Bai, Guiyou Liang","doi":"10.1080/15384101.2025.2485834","DOIUrl":"https://doi.org/10.1080/15384101.2025.2485834","url":null,"abstract":"Exosomes secreted by mesenchymal stem cells (MSCs) have been considered as a novel biological therapy for myocardial ischemia/reperfusion injury (MIRI). However, the underlying mechanism of exosomes has not been completely established, especially in the early stage of MIRI. In this study, we primarily investigated the protective effect of exosomes on MIRI from both in vitro and ex vivo perspectives. Bioinformatic analysis was conducted to identify exosomal miRNA associated with myocardial protection, Genes and proteins related to functional studies and myocardial energy metabolism were analyzed and evaluated using techniques such as Polymerase Chain Re-action (PCR), Western blotting, double luciferase biochemical techniques, flow cytometry assay, etc. It was discovered that exosomes ameliorated cardiomyocyte injury t by delivery of miR-132-3p.This process reduced the expression of Phosphatase and tensin homolog (PTEN) mRNA and protein, enhanced the expression of phosphorylated protein kinase (pAKT), regulated the insulin signaling pathway, facilitated intracellular Glucose transporter 4 (GLUT4) protein membrane translocation, and enhanced glucose uptake and Adenosine Triphosphate (ATP) production. This study confirmed, for the first time, that MSC-EXO can provide myocardial protection in the early stages of MIRI through miR-132/PTEN/AKT pathway. This research establishes a theoretical and experimental foundation for the clinical application of MSC-derived exosomes.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-20"},"PeriodicalIF":3.4,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Non-canonical functions of BCL-2 family members in energy metabolism and necrotic cell death regulation. BCL-2家族成员在能量代谢和坏死细胞死亡调控中的非规范功能。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-03-27 DOI: 10.1080/15384101.2025.2484868

Mohamed El-Mesery, Franziska Rudolf, Yannick Heimann, Georg Häcker, Thomas Brunner

引用次数: 0

Expression of Concern: ATM-dependent phosphorylation of heterogeneous nuclear ribonucleoprotein K promotes p53 transcriptional activation in response to DNA damage. 关注表达：异质核核糖核蛋白K的atm依赖磷酸化促进p53转录激活，以响应DNA损伤。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-03-27 DOI: 10.1080/15384101.2025.2463772

引用次数: 0

Statement of Retraction: Fascin1 mediated release of pro-inflammatory cytokines and invasion/migration in rheumatoid arthritis via the STAT3 pathway. 结论：在类风湿关节炎中，通过STAT3通路，Fascin1介导促炎细胞因子的释放和侵袭/迁移。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-03-26 DOI: 10.1080/15384101.2025.2460937

引用次数: 0

Recent advances in unveiling cellular host-Zika virus interactions in Drosophila. 揭示果蝇细胞宿主-寨卡病毒相互作用的最新进展。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-03-23 DOI: 10.1080/15384101.2025.2482481

Ghada Tafesh-Edwards, Ioannis Eleftherianos

引用次数: 0

c-Jun and Fra-2 pair up to Myc-anistically drive HCC. c-Jun 和 Fra-2 配对，以 Myc-anistically 驱动 HCC。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-11-24 DOI: 10.1080/15384101.2024.2429968

Latifa Bakiri, Erwin F Wagner

{"title":"c-Jun and Fra-2 pair up to Myc-anistically drive HCC.","authors":"Latifa Bakiri, Erwin F Wagner","doi":"10.1080/15384101.2024.2429968","DOIUrl":"https://doi.org/10.1080/15384101.2024.2429968","url":null,"abstract":"Hepatocellular carcinoma (HCC), a leading cause of cancer-related death with limited therapies, is a complex disease developing in a background of Hepatitis Virus infection or systemic conditions, such as the metabolic syndrome. Investigating HCC pathogenesis in model organisms is therefore crucial for developing novel diagnostic and therapeutic tools. Genetically engineered mouse models (GEMMs) have been instrumental in recapitulating the local and systemic features of HCC. Early studies using GEMMs and patient material implicated members of the dimeric Activator Protein-1 (AP-1) transcription factor family, such as c-Jun and c-Fos, in HCC formation. In a recent report, we described how switchable, hepatocyte-restricted expression of a single-chain c-Jun~Fra-2 protein, functionally mimicking the c-Jun/Fra-2 AP-1 dimer, results in spontaneous and largely reversible liver tumors in GEMMs. Dysregulated cell cycle, inflammation, and dyslipidemia are observed at early stages and tumors display molecular HCC signatures. We demonstrate that increased c-Myc expression is an essential molecular determinant of tumor formation that can be therapeutically targeted using the BET inhibitor JQ1. Here, we discuss these findings with additional results illustrating how AP-1 GEMMs can foster preclinical research on liver diseases with novel perspectives offered by the constantly increasing wealth of HCC-related datasets.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-9"},"PeriodicalIF":3.4,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Expression of Concern: DDB2 association with PCNA is required for its degradation after UV-induced DNA damage. 关注表达：紫外线诱导 DNA 损伤后，PCNA 的降解需要 DDB2 与 PCNA 结合。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-09-27 DOI: 10.1080/15384101.2024.2396717

引用次数: 0