Cell Cycle最新文献_第5页

Advances in DNA damage repair mechanisms in stem cells and their applications. 干细胞DNA损伤修复机制及其应用研究进展。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-24 DOI: 10.1080/15384101.2025.2576514

Dongxu Wei, Yuhao Chang, Yao Yang, Xuanbai Chen, Shiqi Jin, Kainan Huang, Zeyidan Jiapaer, Xianli Wang

引用次数: 0

Exosomes in hepatocellular carcinoma: involvement in reprogramming the tumor microenvironment for immune evasion, metastasis, angiogenesis, and drug resistance. 肝细胞癌中的外泌体：参与肿瘤微环境的重编程，以促进免疫逃避、转移、血管生成和耐药性。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-11-08 DOI: 10.1080/15384101.2025.2583289

Mahsa Ghasemian-Irani, Shabnam Babaei, Tohid Kazemi

{"title":"Exosomes in hepatocellular carcinoma: involvement in reprogramming the tumor microenvironment for immune evasion, metastasis, angiogenesis, and drug resistance.","authors":"Mahsa Ghasemian-Irani, Shabnam Babaei, Tohid Kazemi","doi":"10.1080/15384101.2025.2583289","DOIUrl":"10.1080/15384101.2025.2583289","url":null,"abstract":"Hepatocellular carcinoma (HCC) is a highly aggressive liver cancer, and its progression is significantly influenced by the tumor microenvironment (TME). Tumor-derived exosomes (TEXs), an important component of the TME, significantly influence tumor growth by regulating immune responses, facilitating metastasis, and enhancing resistance to therapy. These extracellular vesicles (EVs) transport bioactive substances, such as proteins, lipids, and nucleic acids that promote interaction between cells in the TME. Recent research indicates that HCC-derived exosomes can inhibit immune cell activity, specifically in T cells, thus creating an immunosuppressive TME that facilitates tumor immune escape. They also augment metastatic capability by restructuring the extracellular matrix and promoting angiogenesis. Moreover, HCC-derived exosomes have been associated with developing resistance to drug therapy by transferring molecules such as apoptotic signals and oncogenic microRNAs, circRNAs and lncRNA. Understanding how HCC-derived exosomes affect immune modulation, metastasis, and drug resistance could yield innovative therapeutic targets to enhance therapy outcomes. This review focuses on recent research on the diverse functions of TEXs in HCC progression.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"529-551"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918322/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145470676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Epithelial-mesenchymal-associated non-coding RNAs as Breast cancer metastasis biomarkers. 上皮-间质相关非编码rna作为乳腺癌转移的生物标志物。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-18 DOI: 10.1080/15384101.2025.2576512

Nika Asefi, Ahmad Fazilat, Tayebe Oghabi, Narges Jafarbeik Iravani, Keivan Majidzadeh-A, Farkhonde Hasannejad

{"title":"Epithelial-mesenchymal-associated non-coding RNAs as Breast cancer metastasis biomarkers.","authors":"Nika Asefi, Ahmad Fazilat, Tayebe Oghabi, Narges Jafarbeik Iravani, Keivan Majidzadeh-A, Farkhonde Hasannejad","doi":"10.1080/15384101.2025.2576512","DOIUrl":"10.1080/15384101.2025.2576512","url":null,"abstract":"Breast cancer (BC) is identified as a significant cause of cancer mortality in the female population. The recurrence of initial tumors and the metastasis to remote areas of the body are significant factors leading to the mortality linked with BC. Despite the advancements in diagnostic and therapeutic approaches, a comprehensive understanding of the molecular mechanisms underlying metastasis is still unclear, particularly regarding the regulatory role of non-coding RNAs (ncRNAs) in epithelial-mesenchymal transition (EMT). Different categories of ncRNAs, including microRNAs (miRNAs), circular RNAs (circRNAs), and long ncRNAs (lncRNAs), can manage the complex regulatory frameworks of EMT at various levels. Since dysregulation of ncRNAs is associated with key processes in EMT, investigating them as valuable tools for identifying the metastatic potential of tumors at an early stage could significantly increase diagnostic accuracy and improve patient outcomes, particularly in BC. This review aims to bridge this gap by systematically summarizing current insights into the interplay between EMT and various classes of ncRNAs in the context of BC progression. We discuss the molecular pathways through which ncRNAs regulate EMT, their impact on metastasis and explore their potential as diagnostic biomarkers and therapeutic targets. By providing an integrative overview of recent findings, this article highlights unresolved questions and proposes directions for future research, offering a valuable resource for researchers and clinicians involved in breast cancer biology and treatment development.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"440-467"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12710946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145312427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

The curvature code: BCL-w dimers rewire BAX-BCL-2 control of mitochondrial fate and apoptosis. 曲率代码：BCL-w二聚体重新连接BAX-BCL-2对线粒体命运和凋亡的控制。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-12-01 DOI: 10.1080/15384101.2025.2597275

Gaetano Santulli

引用次数: 0

The methyltransferase METTL3 promotes the progression of breast cancer cells via regulating EGF m6A modification. 甲基转移酶METTL3通过调节EGF m6A修饰促进乳腺癌细胞的进展。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-08 DOI: 10.1080/15384101.2025.2570258

Jiaqing Liu, Han Fang, Xinhao Yang, Yi Lu, Enjie Li, Meina Wang, Zhigang Hu

{"title":"The methyltransferase METTL3 promotes the progression of breast cancer cells via regulating EGF m6A modification.","authors":"Jiaqing Liu, Han Fang, Xinhao Yang, Yi Lu, Enjie Li, Meina Wang, Zhigang Hu","doi":"10.1080/15384101.2025.2570258","DOIUrl":"10.1080/15384101.2025.2570258","url":null,"abstract":"Ranking second out of new cancer cases, breast cancer (BRCA) is the leading cause of cancerous death among women globally. Methyltransferase-like 3 (METTL3), as the well-known N6‑methyladenosine (m6A) \"writer\" with catalytic function, regulates cancer progression through specific downstream targets, but its interplay with epidermal growth factor (EGF) signaling in BRCA is poorly defined. Here, we depict a METTL3-m6A-EGF axis in BRCA, where BRCA cell properties were affected by METTL3 through m6A-dependent expression of EGF. We observed the correlation between METTL3 expression in BRCA tissues and negative prognosis through bioinformatics analysis and RT-qPCR. In vitro lentiviral-mediated METTL3 knockdown suppressed proliferation and migration, while the in vivo tumor formation experiment in nude mice validated the tumor-promoting effect of METTL3. Hematoxylin-eosin staining and immunohistochemistry also showed the tumor-promoting effect of METTL3. Mechanistically, METTL3 stabilized EGF mRNA via m6A modification, as evidenced by MeRIP-qPCR and Western blotting. Notably, METTL3 maintains EGF/EGFR signaling, and its overexpression leads to insensitivity to gefitinib and adriamycin. We naturally conclude that METTL3 is a central epigenetic regulator of EGF-driven BRCA progression, providing a rationale for targeting METTL3 to overcome chemotherapeutic resistance.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"605-618"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12710917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145250057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

"Leucine zipper proteins as emerging therapeutic regulators: structural dynamics, disease associations, and novel targeting strategies". 亮氨酸拉链蛋白作为新兴的治疗调节剂：结构动力学、疾病关联和新的靶向策略。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-11-06 DOI: 10.1080/15384101.2025.2585073

Anjali Kumari, Adiba Mussarrat, Manodeep Chakraborty, Ananya Bhattacharjee, Ravi Kumar Rajan

{"title":"\"Leucine zipper proteins as emerging therapeutic regulators: structural dynamics, disease associations, and novel targeting strategies\".","authors":"Anjali Kumari, Adiba Mussarrat, Manodeep Chakraborty, Ananya Bhattacharjee, Ravi Kumar Rajan","doi":"10.1080/15384101.2025.2585073","DOIUrl":"10.1080/15384101.2025.2585073","url":null,"abstract":"Leucine zipper proteins are transcription factors that regulate gene activity through DNA binding and creating stable pairs. They are located in particular tissues and are involved in significant processes like metabolism, immunity, and stress response. The C/EBPβ (CCAAT/Enhancer-Binding Proteins), which is predominantly active in the liver and spleen, regulates metabolism and immune activity. The GILZ (glucocorticoid-induced leucine zipper), which is located in the brain, lungs, immune cells, and reproductive system, may protect against inflammation and stress. Hormonal signals or oxidative stress may cause these proteins to be activated and transported to the nucleus to turn off or turn on the genes. The disruption of balance, such as the loss of GILZ, drives inflammation, which may cause diseases. Therapies include small molecules, peptides, or DNA decoy therapy. The selective control of these proteins via biomarker profiling and targeted tissue delivery has potential in mitigating cancer, inflammatory, and metabolic diseases.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"552-565"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145450780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Integration of a 4-gene risk score model enhances prognostic accuracy in acute myeloid leukemia. 整合4基因风险评分模型可提高急性髓性白血病的预后准确性。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-29 DOI: 10.1080/15384101.2025.2578389

Yiqing Li, Boqi Li, Jie Xiao, Kezhi Huang, Yuchan Liang, Peiting Zeng, Wenjuan Yang, Danian Nie

{"title":"Integration of a 4-gene risk score model enhances prognostic accuracy in acute myeloid leukemia.","authors":"Yiqing Li, Boqi Li, Jie Xiao, Kezhi Huang, Yuchan Liang, Peiting Zeng, Wenjuan Yang, Danian Nie","doi":"10.1080/15384101.2025.2578389","DOIUrl":"10.1080/15384101.2025.2578389","url":null,"abstract":"The clinical outcomes of acute myeloid leukemia (AML) patients exhibit substantial heterogeneity, with relapse posing a formidable challenge. Herein, we developed a risk score model by integrating relapse-related genes through Cox regression analysis. The relapse-related genes were identified via differential gene expression analysis of 15 matched diagnosed and relapsed AML samples retrieved from the Gene Expression Omnibus (GEO) database. These genes include SCN9A, CFH, CD34, and CALCRL. Our findings demonstrate that higher risk scores were significantly associated with an unfavorable ELN2017 risk classification, leukemic transformation, as well as FLT3-ITD and RUNX1 mutations. Conversely, lower risk scores were linked to NPM1 mutation. Patients with higher risk scores had a shorter overall survival (OS). Furthermore, we integrated the risk score model with the European LeukemiaNet (ELN) risk classification to establish a novel composite risk classification scheme. Patients were classified into three new risk groups based on composite risk classification showing significantly distinct OS. In summary, the four-gene risk score holds promise in predicting the OS of AML patients, and the composite risk classification shows greater potential in predicting the outcomes of AML patients. These four genes may represent potential therapeutic targets in the treatment of AML.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"638-654"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12710893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145399984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Influence of bacterial proteins on the host's cell cycle. 细菌蛋白对宿主细胞周期的影响。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-29 DOI: 10.1080/15384101.2025.2577757

Francesca Benedetti, Camila Summers, Robert C Gallo, Davide Zella

引用次数: 0

Mitophagy suppression via lncRNA H19 silencing: a novel strategy to overcome cisplatin resistance in lung adenocarcinoma. lncRNA H19沉默抑制线粒体自噬：克服肺腺癌顺铂耐药的新策略

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-11-05 DOI: 10.1080/15384101.2025.2581634

Meng-Zhen Liu, Xiao-Yan Shao, Si-Han Wu, Qi-Qi Ning, Can Zhang, Wei-Wei Du, Rong-Rong Sun, San-Yuan Sun, You-Wei Zhang

{"title":"Mitophagy suppression via lncRNA H19 silencing: a novel strategy to overcome cisplatin resistance in lung adenocarcinoma.","authors":"Meng-Zhen Liu, Xiao-Yan Shao, Si-Han Wu, Qi-Qi Ning, Can Zhang, Wei-Wei Du, Rong-Rong Sun, San-Yuan Sun, You-Wei Zhang","doi":"10.1080/15384101.2025.2581634","DOIUrl":"10.1080/15384101.2025.2581634","url":null,"abstract":"Cisplatin (DDP) resistance substantially compromises treatment efficacy in lung adenocarcinoma (LUAD). This study investigates the role of mitochondrial long non-coding RNA (lncRNA) H19 in mediating DDP resistance. High-throughput sequencing and RT-qPCR analyses revealed pronounced H19 upregulation in DDP-resistant A549 (A549/DDP) cells relative to parental A549 cells. Subcellular localization studies indicated that H19 is primarily nuclear in A549 cells but translocates to mitochondria in A549/DDP cells. Functional assays demonstrated that H19 silencing in resistant cells attenuated chemoresistance, suppressed proliferation, migration, invasion, and colony formation in vitro, and delayed tumor growth in vivo. H19 knockdown impaired mitophagy and promoted apoptosis, mirroring autophagy inhibition and restoring DDP sensitivity. In contrast, H19 overexpression in A549 cells did not significantly alter mitophagy or cellular behavior. Furthermore, H19 silencing induced its relocalization from mitochondria back to the nucleus in resistant cells, while overexpression did not affect its nuclear localization. These findings establish that H19 translocation to mitochondria promotes DDP resistance, and its downregulation reverses this process by inhibiting mitophagy and resensitizing cells to DDP. As a nucleus-encoded mitochondria-associated lncRNA (ntmtlncRNA), H19 mediates intercompartmental communication, highlighting its potential as a therapeutic target for overcoming DDP resistance in LUAD.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"670-686"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145450771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

CKS2 promotes the malignant phenotypes of bladder cancer cells via PI3K/AKT signaling pathway activation. CKS2通过激活PI3K/AKT信号通路促进膀胱癌细胞的恶性表型。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-11-07 DOI: 10.1080/15384101.2025.2586117

Tao Yang, Shao-Peng Kong, Qing-Le Xu, Cheng-Xin Zhan, Xiao-Tong Wang, Shou-Bin Li, Gang Wang, Jian-Guo Ma

{"title":"CKS2 promotes the malignant phenotypes of bladder cancer cells via PI3K/AKT signaling pathway activation.","authors":"Tao Yang, Shao-Peng Kong, Qing-Le Xu, Cheng-Xin Zhan, Xiao-Tong Wang, Shou-Bin Li, Gang Wang, Jian-Guo Ma","doi":"10.1080/15384101.2025.2586117","DOIUrl":"10.1080/15384101.2025.2586117","url":null,"abstract":"Cyclin-dependent kinase subunit 2 (CKS2) has been implicated in various malignancies. This study investigates the mechanism by which CKS2 contributes to bladder cancer (BC) progression. Abnormally expressed genes were identified by differential analysis of tumor and normal tissues using Gene Expression Omnibus datasets. Subsequently, functional assays - including cell proliferation, Transwell migration, colony formation, wound healing, flow cytometry, and enzyme-linked immunosorbent assays - were performed to provide cellular evidence supporting the oncogenic function of CKS2 in BC. The results demonstrated significantly elevated CKS2 expression in BC cells than in normal urothelial cells. CKS2 overexpression promoted cell proliferation, cell migration and invasion. Mechanistically, CKS2 overexpression caused a marked reduction in PTEN protein levels, thereby inhibiting PIP3 degradation and indirectly activating the PI3K/AKT signaling pathway. Furthermore, CKS2 promoted phosphorylation and degradation of p27 Kip1 (Thr187), consequently contributing to cell cycle deregulation and further enhancing PI3K/AKT pathway activity. In contrast, CKS2 knockdown produced the opposite effects. Notably, treatment with the PI3K inhibitor LY294002 effectively reversed CKS2-induced BC cell proliferation and metastasis. In conclusion, CKS2 promoted the malignant phenotypes of BC cells by enhancing PI3K/AKT pathway activity through dual mechanisms involving PTEN downregulation and p27 Kip1-mediated cell cycle dysregulation.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"687-701"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145457695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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