Cell Cycle最新文献

{"title":"LncRNA ABHD11-AS1 activates EGFR signaling to promote cervical cancer progression by preventing FUS-mediated degradation of ABHD11 mRNA.","authors":"Ting Yang, Sijuan Tian, Juan Zhao, Meili Pei, Minyi Zhao, Xiaofeng Yang","doi":"10.1080/15384101.2023.2297591","DOIUrl":"10.1080/15384101.2023.2297591","url":null,"abstract":"<p><p>Cervical cancer is one of the most common gynecological cancers with high metastasis, poor prognosis and conventional chemotherapy. The long non-coding RNA (lncRNA) ABHD11 antisense RNA 1 (ABHD11-AS1) plays a vital role in tumorigenesis and is involved in cell proliferation, differentiation, and apoptosis. Especially for cervical cancer, the functions and mechanisms of ABHD11-AS1 are still undetermined. In this study, we explored the role and underlying mechanism of ABHD11-AS1 in cervical cancer. We found that ABHD11-AS1 is highly expressed in cervical cancer tissue. The roles of ABHD11-AS1 and EGFR have investigated the loss of function analysis and cell movability in SiHa and Hela cells. Knockdown of ABHD11-AS1 and EGFR significantly inhibited the proliferation, migration, and invasion and promoted apoptosis of SiHa and Hela cells by up-regulating p21 and Bax and down-regulating cyclin D1, Bcl2, MMP9, and Vimentin. ABHD11-AS1 knockdown could decrease the expression of EGFR. In addition, ABHD11-AS1 could regulate the EGFR signaling pathway, including p-EGFR, p-AKT, and p-ERK. Spearman's correlation analysis and cell experiments demonstrated that ABHD11 was highly expressed in tumor tissue and partially offset the effect of shABHD11-AS1 on the proliferation, migration, and invasion of SiHa and Hela cells. Then, RNA pulldown was used to ascertain the mechanisms of ABHD11-AS1 and FUS. ABHD11-AS1 inhibited ABHD11 mRNA degradation by bounding to FUS. A subcutaneous xenograft of SiHa cells was established to investigate the effect of ABHD11-AS1 in tumor tissue. Knockdown of ABDH11-AS1 inhibited tumor growth and decreased the tumor volume. ABHD11-AS1 knockdown inhibited the expression of Ki67 and Vimentin and up-regulated the expression of Tunel. Our data indicated that ABHD11-AS1 promoted cervical cancer progression by activating EGFR signaling, preventing FUS-mediated degradation of ABHD11 mRNA. Our findings provide novel insights into the potential role of lncRNA in cervical cancer therapy.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"2538-2551"},"PeriodicalIF":4.3,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936639/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139037369","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}

{"title":"m⁶A-mediated lncRNA MAPKAPK5-AS1 induces apoptosis and suppresses inflammation via regulating miR-146a-3p/SIRT1/NF-κB axis in rheumatoid arthritis.","authors":"Jianting Wen, Jian Liu, Lei Wan, Hui Jiang, Ling Xin, Yue Sun, Yanyan Fang, Xin Wang, Jie Wang","doi":"10.1080/15384101.2024.2302281","DOIUrl":"10.1080/15384101.2024.2302281","url":null,"abstract":"<p><p>To investigate the role of m⁶A-mediated lncRNA MAPKAPK5-AS1 (MK5-AS1) in rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs) and its underlying molecular mechanism. RT-qPCR, western blot, flow cytometry (FCM), and enzyme-linked immunosorbent assay (ELISA) were utilized for evaluating inflammation and apoptosis. Next, RIP, RNA pull-down, dual-luciferase reporter gene assay, and a series of rescue experiments were performed to explore the regulatory mechanisms of MK5-AS1 and its sponge-like action in RA-FLSs. The regulatory relationships between MK5-AS1 and WTAP were explored using the MeRIP-qPCR assay and RT-qPCR. Finally, the critical RNAs in the ceRNA axis were verified in the clinical cohort. MK5-AS1 was poorly expressed and miR-146a-3p was overexpressed in co-cultured RA-FLSs. MK5-AS1 overexpression could inhibit inflammatory responses and promote cell apoptosis in the co-cultured RA-FLSs. MK5-AS1 bound to miR-146a-3p to target SIRT1, thereby affecting inflammatory responses and cell apoptosis in the co-cultured RA-FLSs. SIRT1 knockdown or miR-146a-3p overexpression reversed the impacts of MK5-AS1 overexpression on co-cultured RA-FLSs inflammation and apoptosis. Moreover, WTAP was downregulated, and induced the inhibition of MK5-AS1 by promoting its RNA transcript stability. Clinically, MK5-AS1 was downregulated in RA-PBMCS and correlated with the clinical characteristics of RA. Our study elucidated that m⁶A-mediated MK5-AS1 sequestered miR-146a-3p to suppress SIRT1 expression in co-cultured RA-FLSs, thus providing a new insight into the treatment of rheumatoid arthritis.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"2602-2621"},"PeriodicalIF":3.4,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139471888","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}

{"title":"TACC3: a multi-functional protein promoting cancer cell survival and aggressiveness.","authors":"Ozge Saatci, Ozgur Sahin","doi":"10.1080/15384101.2024.2302243","DOIUrl":"10.1080/15384101.2024.2302243","url":null,"abstract":"<p><p>TACC3 is the most oncogenic member of the transforming acidic coiled-coil domain-containing protein (TACC) family. It is one of the major recruitment factors of distinct multi-protein complexes. TACC3 is localized to spindles, centrosomes, and nucleus, and regulates key oncogenic processes, including cell proliferation, migration, invasion, and stemness. Recently, TACC3 inhibition has been identified as a vulnerability in highly aggressive cancers, such as cancers with centrosome amplification (CA). TACC3 has spatiotemporal functions throughout the cell cycle; therefore, targeting TACC3 causes cell death in mitosis and interphase in cancer cells with CA. In the clinics, TACC3 is highly expressed and associated with worse survival in multiple cancers. Furthermore, TACC3 is a part of one of the most common fusions of FGFR, FGFR3-TACC3 and is important for the oncogenicity of the fusion. A detailed understanding of the regulation of TACC3 expression, its key partners, and molecular functions in cancer cells is vital for uncovering the most vulnerable tumors and maximizing the therapeutic potential of targeting this highly oncogenic protein. In this review, we summarize the established and emerging interactors and spatiotemporal functions of TACC3 in cancer cells, discuss the potential of TACC3 as a biomarker in cancer, and therapeutic potential of its inhibition.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"2637-2655"},"PeriodicalIF":3.4,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936615/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139402029","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}

{"title":"The role of CSTF2 in cancer: from technology to clinical application.","authors":"Jiaxiang Ding, Yue Su, Youru Liu, Yuanyuan Xu, Dashuai Yang, Xuefeng Wang, Shuli Hao, Huan Zhou, Hongtao Li","doi":"10.1080/15384101.2023.2299624","DOIUrl":"10.1080/15384101.2023.2299624","url":null,"abstract":"<p><p>A protein called cleavage-stimulating factor subunit 2 (CSTF2, additionally called CSTF-64) binds RNA and is needed for the cleavage and polyadenylation of mRNA. CSTF2 is an important component subunit of the cleavage stimulating factor (CSTF), which is located on the X chromosome and encodes 557 amino acids. There is compelling evidence linking elevated CSTF2 expression to the pathological advancement of cancer and on its impact on the clinical aspects of the disease. The progression of cancers, including hepatocellular carcinoma, melanoma, prostate cancer, breast cancer, and pancreatic cancer, is correlated with the upregulation of CSTF2 expression. This review provides a fresh perspective on the investigation of the associations between CSTF2 and various malignancies and highlights current studies on the regulation of CSTF2. In particular, the mechanism of action and potential clinical applications of CSTF2 in cancer suggest that CSTF2 can serve as a new biomarker and individualized treatment target for a variety of cancer types.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"2622-2636"},"PeriodicalIF":3.4,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936678/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139080497","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}

{"title":"Identification of molecular subtypes and prognostic model to reveal immune infiltration and predict prognosis based on immunogenic cell death-related genes in lung adenocarcinoma.","authors":"Yinying Dong, Xiao Yu, Hao Song, Qingfeng Chen, Bin Zheng, Xiaomeng Ji, Mingjin Xu, Jian Liu, Xiangyin Sun, Qiuxiao Wang, Ruimei Ren, Haijun Lu","doi":"10.1080/15384101.2023.2300591","DOIUrl":"10.1080/15384101.2023.2300591","url":null,"abstract":"<p><p>Immunogenic cell death (ICD) has been increasingly indicated to be related to caners. However, ICD's role in Lung adenocarcinoma (LUAD) is still not well investigated. Clinical data along with associated mRNA expression profiles from LUAD cases were collected in TCGA and GEO databases. 13 ICD-related genes were identified. Relations of ICD-related genes expression with prognosis of patients, tumor immune microenvironment (TIME) was analyzed. Then, candidate genes were identified and the prognostic signature were constructed. Afterwards, one nomogram incorporating those chosen clinical data together with risk scores were built. Finally, the effect of HSP90AA1, one gene of the prognostic signature, on LUAD cell were analyzed. Two clusters were identified, which were designated as the ICD-high or -low subtype according to ICD-related genes levels. ICD-high subgroup showed good prognosis, high immune cell infiltration degrees, and enhanced immune response signaling activity compared with ICD-low subtype. Moreover, we established and verified the risk signature based on ICD-related genes. High risk group predicted poor prognosis of LUAD independently and presented negative association with immune score and immune status. Furthermore, nomogram contributed to the accurate prediction of LUAD prognostic outcome. Finally, HSP90AA1 levels were remarkably elevated within tumor cells in comparison with healthy pulmonary epithelial cells. HSP90α, HSP90AA1 protein product, promoted growth, migration, and invasion of LUAD cells. Molecular subtypes and prognostic model were identified by incorporating ICD-related genes, and it was related to TIME and might be adopted for the accurate prediction of LUAD prognosis.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"2566-2583"},"PeriodicalIF":3.4,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139073442","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}

{"title":"Telomere dynamics in human pluripotent stem cells.","authors":"Buyun Ma, Paula Martínez, Raúl Sánchez-Vázquez, Maria A Blasco","doi":"10.1080/15384101.2023.2285551","DOIUrl":"10.1080/15384101.2023.2285551","url":null,"abstract":"<p><p>Pluripotent stem cells (PSCs) are a promising source of stem cells for regenerative therapies. Stem cell function depends on telomere maintenance mechanisms that provide them with the proliferative capacity and genome stability necessary to multiply and regenerate tissues. We show here that established human embryonic stem cells (hESCs) have stable telomere length that is dependent on telomerase but not on alternative mechanisms based on homologous recombination pathways. Here, we show that human-induced pluripotent stem cells (hiPSCs) reprogrammed from somatic cells show progressive telomere lengthening until reaching a length similar to ESCs. hiPSCs also acquire telomeric chromatin marks of ESCs including decreased abundance of tri-methylated histone H3K9 and H4K20 and HP1 heterochromatic marks, as well as of the shelterin component TRF2. These chromatin features are accompanied with increased abundance of telomere transcripts or TERRAs. We also found that telomeres of both hESCs and hiPSCs are well protected from DNA damage during telomere elongation and once full telomere length is achieved, and exhibit stable genomes. Collectively, this study highlights that hiPSCs acquire ESC features during reprogramming and reveals the telomere biology in human pluripotent stem cells (hPSCs).</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"2505-2521"},"PeriodicalIF":4.3,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936660/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139466349","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}

{"title":"Drug-induced inhibition of HMGA and EZH2 activity as a possible therapy for anaplastic thyroid carcinoma.","authors":"Marco De Martino, Simona Pellecchia, Myriam Decaussin-Petrucci, Domenico Testa, Nathalia Meireles Da Costa, Pierlorenzo Pallante, Paolo Chieffi, Alfredo Fusco, Francesco Esposito","doi":"10.1080/15384101.2023.2298027","DOIUrl":"10.1080/15384101.2023.2298027","url":null,"abstract":"<p><p>Anaplastic thyroid carcinoma (ATC) is one of the most aggressive and lethal neoplasms in humans, and just limited progresses have been made to extend patient survival and decrease ATC-associated mortality. Thus, the identification of novel therapeutic strategies for treating ATC is needed. Recently, our group has identified two proteins with oncogenic activity, namely HMGA1 and EZH2, with pivotal roles in ATC cancer progression. Therefore, we tested the ability of trabectedin, a HMGA1-targeting drug, and GSK126, an inhibitor of EZH2 enzymatic activity, to impair cell viability of four ATC-derived cell lines. In the present study, we first confirmed the overexpression of <i>HMGA1</i> and <i>EZH2</i> in all ATC-derived cell lines and tissues compared to the normal primary thyroid cells and tissues. Then, treatment of the ATC cell lines with trabectedin and GSK126 resulted in a drastic induction of apoptotic cell death, which increased when the ATC cell lines were treated with a combination of both drugs. Conversely, normal primary human thyroid cells did not show any significant reduction in their viability when exposed to the same drugs. Noteworthy, both drugs induced the deregulation of <i>EZH2</i>- and <i>HMGA1</i>-controlled genes. Altogether, these findings propose the combination of trabectedin and GSK126 as possible novel strategy for ATC therapy.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"2552-2565"},"PeriodicalIF":3.4,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936675/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139073441","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}

{"title":"The role of lncRNA SNHG14 in gastric cancer: enhancing tumor cell proliferation and migration, and mechanisms of CDH2 expression.","authors":"Zhou-Tong Dai, Yong-Lin Wu, Tao Xu, Xing-Rui Li, Teng Ji","doi":"10.1080/15384101.2023.2289745","DOIUrl":"10.1080/15384101.2023.2289745","url":null,"abstract":"<p><p>LncRNAs are a class of non-coding RNAs that play an important role in regulating gene expression. However, their specific molecular mechanisms in gastric carcinogenesis and metastasis need further exploration. TCGA data showed that the expression of MFGE8, which was closely related to survival, was significantly positively correlated with lncRNA SNHG14. And moreover, the results of high-throughput sequencing and qRT-PCR showed that lncRNA SNHG14 was significantly elevated in gastric cancer. Further, in vitro functional realization showed that lncRNA SNHG14 overexpression significantly increased gastric cancer's proliferation, invasion and migration. Animal experiments also showed that lncRNA SNHG14 overexpression promoted tumorigenesis and metastasis in vivo. Mechanistically, MFGE8 activates the expression of lncRNA SNHG14, which activates the cellular EMT by stabilizing CDH2. Our study suggests that lncRNA SNHG14 could be a potential target for gastric cancer therapy.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"2522-2537"},"PeriodicalIF":3.4,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139402030","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}

{"title":"The mystery of phospho-Drp1 with four adaptors in cell cycle: when mitochondrial fission couples to cell fate decisions.","authors":"Nian-Siou Wu, I-Chu Ma, Yi-Fan Lin, Huey-Jiun Ko, Joon-Khim Loh, Yi-Ren Hong","doi":"10.1080/15384101.2023.2289753","DOIUrl":"10.1080/15384101.2023.2289753","url":null,"abstract":"<p><p>Recent study had deepened our knowledge of the mitochondrial dynamics to classify mitochondrial fission into two types. To further clarify the relationship between the two distinct fission machinery and the four major adaptors of Drp1, we propose a model of mechanism elucidating the multiple functions of phospho-Drp1 with its adaptors during cell cycle and providing in-depth insights into the molecular basis and evolutionary implications in depth. The model highlights not only the clustering characteristics of different phospho-Drp1 with respective subsets of mitochondrial pro-fission adaptors but also the correlation, crosstalk and shifting between different clustering of phosphorylated Drp1-adaptors during different key fission situations. Particularly, phospho-Drp1 (Ser616) couples with Mff/MiD51 to exert mitochondrial division and phospho-Drp1 (Ser637) couples with MiD49/Fis1 to execute mitophagy in M-phase. We then apply the model to address the relationship of mitochondrial dynamics to Parkinson's disease (PD) and carcinogenesis. Our proposed model is indeed compatible with current research results and pathological observations, providing promising directions for future treatment design.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"2485-2503"},"PeriodicalIF":3.4,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10802209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138486760","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}

{"title":"High-density lipoprotein protects vascular endothelial cells from indoxyl sulfate insults through its antioxidant ability.","authors":"Ching Chen, Chia-Chi Chang, I-Ta Lee, Chun-Yao Huang, Feng-Yen Lin, Shing-Jong Lin, Jaw-Wen Chen, Ting-Ting Chang","doi":"10.1080/15384101.2023.2296184","DOIUrl":"10.1080/15384101.2023.2296184","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) patients have a high risk of cardiovascular disease. Indoxyl sulfate (IS) is a uremic toxin that has been shown to inhibit nitric oxide production and cause cell senescence by inducing oxidative stress. High-density lipoprotein (HDL) has a protective effect on the cardiovascular system; however, its impacts on IS-damaged endothelial cells are still unknown. This study aimed to explore the effects of exogenous supplement of HDL on vascular endothelial cells in a uremia-mimic environment. Tube formation, migration, adhesion, and senescence assays were used to evaluate the cell function of human aortic endothelial cells (HAECs). Reactive oxygen species generation was measured by using Amplex red assay. L-NAME and MCI186 were used as a nitric oxide synthase inhibitor and a free radical scavenger, respectively. HDL exerted anti-inflammatory and antioxidant effects via HIF-1α/HO-1 activation and IL-1β/TNF-α/IL-6 inhibition in IS-stimulated HAECs. HDL improved angiogenesis ability through upregulating Akt/eNOS/VEGF/SDF-1 in IS-stimulated HAECs. HDL decreased endothelial adhesiveness via downregulating VCAM-1 and ICAM-1 in IS-stimulated HAECs. Furthermore, HDL reduced cellular senescence via upregulating SIRT1 and downregulating p53 in IS-stimulated HAECs. Importantly, the above beneficial effects of HDL were mainly due to its antioxidant ability. In conclusion, HDL exerted a comprehensive protective effect on vascular endothelial cells against damage from IS through its antioxidant ability. The results of this study might provide a theoretical basis for potential HDL supplementation in CKD patients with endothelial damage.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"2409-2423"},"PeriodicalIF":3.4,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10802207/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138828339","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}