Cell Cycle最新文献_第2页

TimeVault turns vault particles into molecular memory of transcriptional states: how to decode the cellular black box. TimeVault将vault粒子转化为转录状态的分子记忆：如何解码细胞黑盒子。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-03-06 DOI: 10.1080/15384101.2026.2639760

Gaetano Santulli

{"title":"TimeVault turns vault particles into molecular memory of transcriptional states: how to decode the cellular black box.","authors":"Gaetano Santulli","doi":"10.1080/15384101.2026.2639760","DOIUrl":"10.1080/15384101.2026.2639760","url":null,"abstract":"Cellular phenotypes are shaped not only by current molecular states but by transient transcriptional programs that encode prior experiences and influence future behavior. Conventional transcriptomic approaches, including bulk and single-cell RNA sequencing, provide high-resolution snapshots of gene expression but are intrinsically destructive, precluding direct linkage between past transcriptional states and downstream cellular fate. In this context, \"TimeVault\" introduces a fundamentally new paradigm by enabling intracellular storage of endogenous transcriptomes within living cells. By repurposing vault ribonucleoprotein particles to sequester and stabilize polyadenylated mRNA, TimeVault preserves unbiased, transcriptome-wide records of transcriptional states over timescales far exceeding native mRNA half-lives. This capability allows retrospective reconstruction of molecular histories that would otherwise be lost, bridging a critical gap between transient gene expression and long-term phenotypic outcomes. Application of TimeVault to canonical stress responses demonstrates precise temporal gating and durable transcript preservation, while its use in cancer models reveals preexisting transcriptional programs that predict drug-tolerant persister cell formation prior to therapy. These findings highlight the power of molecular memory devices to uncover causal relationships that remain invisible to conventional endpoint analyses. TimeVault establishes intracellular transcriptome archiving as a versatile tool with broad implications for developmental biology, stress adaptation, and therapeutic resistance.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-4"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12969733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147364072","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

MicroRNA-6833-3p drives prostate cancer progression and stemness by targeting the NUMB-mediated NOTCH signaling pathway. MicroRNA-6833-3p通过靶向numb介导的NOTCH信号通路驱动前列腺癌的进展和干细胞。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-06-23 DOI: 10.1080/15384101.2026.2687838

Kai Wang, Gang Wang, Jia Shao, Changjiu Li, Sihan Wang, Hongshen Wu, Huadong He

{"title":"MicroRNA-6833-3p drives prostate cancer progression and stemness by targeting the NUMB-mediated NOTCH signaling pathway.","authors":"Kai Wang, Gang Wang, Jia Shao, Changjiu Li, Sihan Wang, Hongshen Wu, Huadong He","doi":"10.1080/15384101.2026.2687838","DOIUrl":"10.1080/15384101.2026.2687838","url":null,"abstract":"Understanding molecular pathways in prostate cancer (PCa) is essential. This study demonstrates that miR-6833-3p plays a key role in prostate tumorigenesis via multi-omics integration and functional validation. Expression levels of miR-6833-3p, NUMB, and NOTCH1 were measured in PCa cell lines. The direct regulation of NUMB by miR-6833-3p was confirmed via dual-luciferase reporter assays with mutagenesis. Functional effects were examined using NUMB plasmids or miR-6833-3p mimics. Cell function assays and xenograft models in nude mice were employed, with tissues analyzed via HE staining, qRT-PCR, and Western blot. miR-6833-3p and NOTCH1 were upregulated in PCa, while NUMB was downregulated. miR-6833-3p mimics promoted proliferation, migration, and stemness but inhibited apoptosis and the NUMB/NOTCH1 pathway. NUMB overexpression reversed these effects. In vivo, miR-6833-3p accelerated tumor growth and suppressed NUMB/NOTCH1. miR-6833-3p promotes PCa progression and stemness by inhibiting the NUMB-NOTCH pathway, highlighting its potential as a biomarker for detection and targeted therapy.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-14"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13313279/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148301149","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

Circular RNA circ_0001829 attenuates G2/M arrest to promote hepatocyte proliferation by sponging miR-3095-3p following liver injury. 环状RNA circ_0001829减弱G2/M阻滞，通过海绵miR-3095-3p促进肝损伤后肝细胞增殖。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-06-28 DOI: 10.1080/15384101.2026.2694138

He Tong, Sarina Wang, Jing Shi, Haiting Pan, Pengxia Liu, Li Wang

{"title":"Circular RNA circ_0001829 attenuates G2/M arrest to promote hepatocyte proliferation by sponging miR-3095-3p following liver injury.","authors":"He Tong, Sarina Wang, Jing Shi, Haiting Pan, Pengxia Liu, Li Wang","doi":"10.1080/15384101.2026.2694138","DOIUrl":"10.1080/15384101.2026.2694138","url":null,"abstract":"Circular RNAs (circRNAs), a class of non-coding RNAs, are critical regulators of liver injury repair. In this study, using a CCl4-induced mouse liver injury model, we conducted high-throughput sequencing to identify circRNAs enriched in the cell cycle pathway. Four circRNAs (circ_0000604, circ_0001350, circ_0001829, and circ_0001830) were significantly upregulated in early liver injury, with dynamic expression patterns closely linked to repair. Of these, circ_0001829 was selected for functional validation. Circ_0001829 overexpression promoted FL83B cell proliferation and alleviated G2/M phase arrest, whereas its knockdown inhibited these effects. This pro-proliferative effect was confirmed in Hepa1-6 cells. Mechanistically, circ_0001829 functions as a molecular sponge for miR-3095-3p, attenuating its repression of the target gene CDC7 and forming a novel competitive endogenous RNA (ceRNA) axis: circ_0001829/miR-3095-3p/CDC7. To the best of our knowledge, this is the first study to demonstrate that circ_0001829 facilitates liver injury repair by promoting cell proliferation and mitigating cell cycle arrest via a ceRNA mechanism. These results offer valuable insights for the development of ncRNA-based therapeutics for liver injury.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-15"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13321877/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148344093","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 effect of energy metabolism on embryonic development and endometrial receptivity in patients with repeated implantation failure. 反复着床失败患者能量代谢对胚胎发育和子宫内膜容受性的影响。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-07-29 DOI: 10.1080/15384101.2026.2709169

Mingyan Jiang, Yuanyuan Li, Yiting Chen, Ting Yu, Qingxin Xu, Peiyi Wu, Tingting Yang

{"title":"The effect of energy metabolism on embryonic development and endometrial receptivity in patients with repeated implantation failure.","authors":"Mingyan Jiang, Yuanyuan Li, Yiting Chen, Ting Yu, Qingxin Xu, Peiyi Wu, Tingting Yang","doi":"10.1080/15384101.2026.2709169","DOIUrl":"10.1080/15384101.2026.2709169","url":null,"abstract":"Repeated implantation failure (RIF) remains a formidable challenge in in vitro fertilization-embryo transfer (IVF-ET). The etiology of RIF is multifactorial, involving complex interactions between embryo quality, the endometrium, and the maternal microenvironment. Adequate energy metabolism is pivotal for successful embryo implantation, supporting both embryonic development and the establishment of endometrial receptivity. Conversely, metabolic dysregulation contributes to RIF by arresting embryonic development, impairing endometrial receptivity, and disrupting the essential crosstalk between the embryo and the endometrium. Embryos and endometrial tissues from patients with RIF frequently exhibit distinct metabolomic abnormalities, including glycolysis utilization disorders, lipid metabolism disorders, and mitochondrial dysfunction. Clinical evidence suggests that therapeutic interventions involving antioxidants and specific metabolic modulators can enhance pregnancy rates in this population. This article reviews the critical role of energy metabolism in embryonic development and implantation, elucidates the pathological mechanisms linking metabolic dysfunction to RIF, and explores potential therapeutic strategies. We highlight that a comprehensive management strategy integrating diet, exercise, and targeted nutritional and antioxidant supplementation is expected to restore metabolic homeostasis in RIF patients and improve reproductive outcomes.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-20"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13432838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148599527","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

KCMF1 promotes malignant progression by NXN ubiquitin-dependent degradation in ovarian cancer. KCMF1通过卵巢癌中NXN泛素依赖性降解促进恶性进展。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-02-21 DOI: 10.1080/15384101.2026.2630888

Xinyu Xu, Ling Ouyang, Jiayuan Wang, Yan Dong, Xiaochuan Yu, Ju Zhou, Meng Jiang

{"title":"KCMF1 promotes malignant progression by NXN ubiquitin-dependent degradation in ovarian cancer.","authors":"Xinyu Xu, Ling Ouyang, Jiayuan Wang, Yan Dong, Xiaochuan Yu, Ju Zhou, Meng Jiang","doi":"10.1080/15384101.2026.2630888","DOIUrl":"10.1080/15384101.2026.2630888","url":null,"abstract":"Ovarian cancer, one of the most lethal gynecologic malignancies, exhibits marked tumor heterogeneity. Potassium channel modulatory factor 1 (KCMF1), a RING zinc-finger protein with E3 ubiquitin ligase activity, has been implicated in tumorigenesis. However, the role of KCMF1 in ovarian cancer remains unclear. In this study, we found that KCMF1 was up-regulated in ovarian cancer tissues and that high KCMF1 expression correlated with poor survival of patients. Functional assays revealed that KCMF1 knockdown suppressed cell viability, hampered cell cycle progression, and inhibited proliferation in ovarian cancer cells. Moreover, silencing KCMF1 inhibited epithelial-mesenchymal transition (EMT), migration, and invasion in vitro. In vivo experiments confirmed that KCMF1 knockdown inhibited tumor growth and metastasis in nude mice. Conversely, KCMF1 overexpression had opposite effects in vitro and in vivo. IP-LC/MS and Label-free proteomic analysis identified nucleoredoxin (NXN), a multifunctional redox-active protein, as a potential substrate of KCMF1. Silencing NXN facilitated cell proliferation, migration, and invasion through activating the β-catenin signaling pathway. Mechanistically, we discovered that KCMF1 interacted with NXN and facilitates its degradation through K63-linked ubiquitination, thereby reducing NXN expression. Taken together, our study showed that KCMF1 promotes ovarian cancer progression through NXN, and KCMF1 might be a novel target for ovarian cancer therapy.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-19"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146257281","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

Stattic administration plays a protective role in a lipopolysaccharide-induced acute lung injury cell model. 静态给药对脂多糖诱导的急性肺损伤细胞模型具有保护作用。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-06-08 DOI: 10.1080/15384101.2026.2683323

Bingshu Li, Chenchen Liu, Huanxia Li, Yujin Sun, Ranran Zhang, Fengjin Liu, Qin Song, Yonglei Zhang

{"title":"Stattic administration plays a protective role in a lipopolysaccharide-induced acute lung injury cell model.","authors":"Bingshu Li, Chenchen Liu, Huanxia Li, Yujin Sun, Ranran Zhang, Fengjin Liu, Qin Song, Yonglei Zhang","doi":"10.1080/15384101.2026.2683323","DOIUrl":"10.1080/15384101.2026.2683323","url":null,"abstract":"Inflammation and apoptosis are vital the processesis of acute lung injury (ALI). Signal transducer and activator of transcription 3 (Stat3) plays diverse roles in cellular processes. Little is known about the activation and function of lungs during ALI. Stat3 activation is observed during ALI. RAW264.7 cells were treated with lipopolysaccharide (LPS) to establish an ALI cell model. Stattic, a Stat3 inhibitor, was then administered to LPS-treated RAW264.7, to probe its effect on inflammation, apoptosis, and oxidative stress in vitro. Western blot analysis confirmed that Stat3 was upregulated and phosphorylated in LPS-exposed cells, while stattic administration decreased these effects. LPS treatment reduced cell viability, as evidenced by MTT, CCK-8, and colony formation assays. However, cell viability was restored after treatment with stattic. ELISA and quantitative PCR indicated that pro-inflammation cytokines, such as Interleukin-1β, IL-6, IL-8, matrix metalloproteinase-13, and tumor necrosis factor-α, were robustly elevated due to LPS stimulation; however, stattic treatment abolished the upregulation of these cytokines. Furthermore, analysis of oxidative stress effectors (malondialdehyde, glutathione, catalase, and superoxide dismutase) showed that LPS treatment upregulated oxidative stress, which was confirmed by the deactivation of the Kelch-like ECH-associated protein 1/nuclear factor erythroid 2-related factor 2/heme oxygenase-1/NAD(P)H quinone dehydrogenase 1 pathway. Apoptosis in cells was also upregulated by LPS. Stattic alleviated oxidative stress and apoptosis induced by LPS. Moreover, Stat3 overexpression reversed the protective effects of stattic on cell viability, inflammation, oxidative stress, and apoptosis. Our study demonstrates that stattic treatment mitigates LPS-triggered inflammatory injury by deactivating the Jak1/Stat3 pathway in ALI.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-11"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13248907/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197321","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 two faces of Rb: from cell-cycle brake to transcriptional driver of CDK4/6 inhibitor resistance. Rb的两面：从细胞周期刹车到CDK4/6抑制剂耐药的转录驱动。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-09-15 DOI: 10.1080/15384101.2026.2733564

Gaetano Santulli

引用次数: 0

Correction. 修正。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2025-12-22 DOI: 10.1080/15384101.2025.2607788

引用次数: 0

Control of DNA double-strand break repair by the KDM8 histone demethylase. KDM8组蛋白去甲基化酶控制DNA双链断裂修复。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-04-19 DOI: 10.1080/15384101.2026.2659192

Jérémie Fages, Valérie Bergoglio, Emmanuel Julia, Luana Cintori, Catherine Chailleux, Anne-Lise Fourez, Natacha Ponsolle, Didier Trouche, Yvan Canitrot

{"title":"Control of DNA double-strand break repair by the KDM8 histone demethylase.","authors":"Jérémie Fages, Valérie Bergoglio, Emmanuel Julia, Luana Cintori, Catherine Chailleux, Anne-Lise Fourez, Natacha Ponsolle, Didier Trouche, Yvan Canitrot","doi":"10.1080/15384101.2026.2659192","DOIUrl":"10.1080/15384101.2026.2659192","url":null,"abstract":"KDM8 is a histone demethylase initially characterized for its activity on H3K36me2, although its function is now more widely recognized as a hydroxylase. Through a high-throughput screening on histone demethylases, we identified KDM8 as a regulator of the γH2AX response following ionizing radiation. Experiments using specific reporter substrates revealed that KDM8 depletion increases homologous recombination (HR), while its overexpression reduces HR. This shift is counterbalanced by a concomitant decrease in non-homologous end joining (NHEJ), an effect partly independent of its demethylase activity and unrelated to cell cycle alterations. Despite this imbalance, cellular sensitivity to DNA-damaging agents - such as ionizing radiation, mitomycin C, and camptothecin - remains unchanged. FRET experiments in living cells demonstrated an interaction between KDM8 and Rad51 after DNA damage induced by camptothecin. These findings identify KDM8 as a key player in DSB repair, specifically influencing HR.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-14"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13094220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721816","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

Dysregulation of the Cyclin D/E2F activity as a core mechanism driving cancer stem cell plasticity and cell cycle dynamics. Cyclin D/E2F活性失调是驱动癌症干细胞可塑性和细胞周期动力学的核心机制。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2025-12-14 DOI: 10.1080/15384101.2025.2599081

Yasin Ahmadi, Trefa Mohammed, Sakhavat Abolhasani, Shwan Abdullah Hamad, Tahran Faiq

{"title":"Dysregulation of the Cyclin D/E2F activity as a core mechanism driving cancer stem cell plasticity and cell cycle dynamics.","authors":"Yasin Ahmadi, Trefa Mohammed, Sakhavat Abolhasani, Shwan Abdullah Hamad, Tahran Faiq","doi":"10.1080/15384101.2025.2599081","DOIUrl":"10.1080/15384101.2025.2599081","url":null,"abstract":"Cancer stem cells (CSCs) represent a highly specialized intratumoral compartment responsible for tumor initiation, metastatic dissemination, therapeutic resistance, and disease recurrence. A central conceptual challenge in CSC biology is their capacity to oscillate between a quiescent G0 state and a proliferative, stem-like phenotype, reflecting a high degree of phenotypic plasticity. Although dysregulation of the G1/S checkpoint is a hallmark of malignant transformation, its mechanistic contribution to CSC identity and plastic behavior remains poorly defined.This review outlines a conceptual model that integrates aberrant G1/S control with CSC state transitions. We propose that defective checkpoint regulation accelerates CSC proliferation, leading to the progressive intracellular accumulation of Cyclin D, which in turn drives a self-reinforcing, rapid G1 progression through phosphorylation-dependent pathways that operate independently of the slower, transcription-driven Cyclin D-Rb-E2F regulatory axis. With continued cycling, depletion of key E2F-regulated DNA replication factors ensues, eventually forcing CSCs into a quiescent, biosynthetic restoration phase. During this interval, essential genomic replication and cell cycle machinery are replenished until microenvironmental or intracellular cues trigger reentry into the proliferative cycle, giving rise to another burst of accelerated division.Through these cyclical perturbations in the Cyclin D/E2F balance, CSCs undergo temporally governed shifts between quiescent and proliferative states, thereby sustaining plasticity, intratumoral heterogeneity, and treatment-resistant phenotypes. This model also identifies potential therapeutic strategies, such as leveraging stimuli-responsive delivery systems that exploit cyclic CSC vulnerabilities.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-29"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145755134","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