Cell Cycle最新文献

{"title":"Extracellular vesicles from <i>Fusobacterium nucleatum</i>: roles in the malignant phenotypes of gastric cancer.","authors":"Xiangkun Meng, Gang Ma, Xu Zhang, Hua Yin, Yu Miao, Fang He","doi":"10.1080/15384101.2024.2324587","DOIUrl":"10.1080/15384101.2024.2324587","url":null,"abstract":"<p><p>The increase of the <i>Fusobacterium nucleatum</i> level has been previously identified in various cancers including gastric cancer (GC), but how the <i>F. nucleatum</i> exerts its carcinogenic role in GC remains unclear. Several studies revealed that <i>F. nucleatum</i> contributes to cancer progression via its secretion of extracellular vehicles (EVs). Hence, it's designed to reveal the influence of <i>F. nucleatum</i>-derived EVs (Fn-EVs) in GC progression. The tumor and adjacent tissues were collected from 30 GC patients, and the abundance of <i>F. nucleatum</i> was found to be highly expressed in tumor samples. The ultracentrifugation was employed to isolate EVs from <i>F. nucleatum</i> and <i>Escherischia coli</i> (<i>E. coli</i>), which were labeled Fn-EVs and <i>E. coli</i>-EVs, respectively. After treating GC cells with Fn-EVs and <i>E. coli</i>-EVs, cell counting kit 8, colony formation, wound healing as well as transwell assay were performed, which revealed that Fn-EVs effectively enhanced oxaliplatin resistance, and facilitated cell proliferation, migration, invasion, and stemness in GC cells while <i>E. coli</i>-EVs exert no significant effect on GC cells. Besides, the stemness and DNA repair of GC cells were also enhanced by Fn-EVs, as revealed by the sphere-forming assay and the detection of stemness- and DNA repair-associated proteins by western blotting. <i>In vivo</i> analyses demonstrated that Fn-EVs administration not only promoted GC tumor growth and liver metastasis but also conferred GC tumor resistance to oxaliplatin resistance. This study first revealed the contributive role of <i>F. nucleatum</i> in GC development via Fn-EVs, which provided a better perspective for manipulating <i>F. nucleatum</i> in treating GC patients with malignant phenotypes.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"294-307"},"PeriodicalIF":3.4,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11057558/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140038750","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":"Hyaluronidase inhibitor sHA2.75 alleviates ischemia-reperfusion-induced acute kidney injury.","authors":"Yang Zhang, Huajiang Zhao, Jing Zhang","doi":"10.1080/15384101.2024.2309019","DOIUrl":"10.1080/15384101.2024.2309019","url":null,"abstract":"<p><p>Hyaluronidases (HAases) are enzymes that degrade hyaluronic acid (HA) in the animal kingdom. The HAases-HA system is crucial for HA homeostasis and plays a significant role in biological processes and extracellular matrix (ECM)-related pathophysiological conditions. This study aims to explore the role of inhibiting the HAases-HA system in acute kidney injury (AKI). We selected the potent inhibitor \"sHA2.75\" to inhibit HAase activity through mixed inhibitory mechanisms. The ischemia-reperfusion mouse model was established using male BALB/c mice (7-9 weeks old), and animals were subjected to subcapsular injection with 50 mg/kg sHA2.75 twice a week to evaluate the effects of sHA2.75 on AKI on day 1, 5 and 14 after ischemia-reperfusion or sham procedure. Blood and tissue samples were collected for immunohistochemistry, biochemical, and quantitative analyses. sHA2.75 significantly reduced blood urea nitrogen (BUN) and serum creatinine levels in AKI mouse models. Expression of kidney injury-related genes such as Kidney injury molecule-1 (KIM-1), Neutrophil Gelatinase-Associated Lipocalin (NGAL), endothelial nitric oxide synthase (eNOS), type I collagen (Col1), type III collagen (Col3), alpha-smooth muscle actin (α-SMA) showed significant downregulation in mouse kidney tissues after sHA2.75 treatment. Moreover, sHA2.75 treatment led to decreased plasma levels of Interleukin-6 (IL-6) proteins and reduced mRNA levels in renal tissues of AKI mice. Inhibitor sHA2.75 administration in the AKI mouse model downregulated kidney injury-related biomarkers and immune-specific genes, thereby alleviating AKI in vivo. These findings suggest the potential use of HAase inhibitors for treating ischemic reperfusion-induced kidney injury.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"248-261"},"PeriodicalIF":3.4,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11057651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140206310","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":"REV7-p53 interaction inhibits ATM-mediated DNA damage signaling.","authors":"Megan Biller, Sara Kabir, Chkylle Boado, Sarah Nipper, Alexandra Saffa, Ariella Tal, Sydney Allen, Hiroyuki Sasanuma, Didier Dréau, Cyrus Vaziri, Junya Tomida","doi":"10.1080/15384101.2024.2333227","DOIUrl":"10.1080/15384101.2024.2333227","url":null,"abstract":"<p><p>REV7 is an abundant, multifunctional protein that is a known factor in cell cycle regulation and in several key DNA repair pathways including Trans-Lesion Synthesis (TLS), the Fanconi Anemia (FA) pathway, and DNA Double-Strand Break (DSB) repair pathway choice. Thus far, no direct role has been studied for REV7 in the DNA damage response (DDR) signaling pathway. Here we describe a novel function for REV7 in DSB-induced p53 signaling. We show that REV7 binds directly to p53 to block ATM-dependent p53 Ser15 phosphorylation. We also report that REV7 is involved in the destabilization of p53. These findings affirm REV7's participation in fundamental cell cycle and DNA repair pathways. Furthermore, they highlight REV7 as a critical factor for the integration of multiple processes that determine viability and genome stability.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"339-352"},"PeriodicalIF":3.4,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11174130/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140334831","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":"Correction.","authors":"","doi":"10.1080/15384101.2024.2317629","DOIUrl":"10.1080/15384101.2024.2317629","url":null,"abstract":"","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"338"},"PeriodicalIF":4.3,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11057576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140206309","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":"Effects of <i>Ninjurin 2</i> polymorphisms on susceptibility to coronary heart disease.","authors":"Yuping Yan, Xiaoyan Du, Xia Dou, Jingjie Li, Wenjie Zhang, Shuangyu Yang, Wenting Meng, Gang Tian","doi":"10.1080/15384101.2024.2330225","DOIUrl":"10.1080/15384101.2024.2330225","url":null,"abstract":"<p><strong>Objective: </strong>The aim of this study was to explore the effects of Ninjurin 2 (NINJ2) polymorphisms on susceptibility to coronary heart disease (CHD).</p><p><strong>Methods: </strong>We conducted a case-control study with 499 CHD cases and 505 age and gender-matched controls. Five single nucleotide polymorphisms (SNPs) in NINJ2 (rs118050317, rs75750647, rs7307242, rs10849390, and rs11610368) were genotyped by the Agena MassARRAY platform. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using logistic regression analysis to assess the association of NINJ2 polymorphisms and CHD risk-adjusted for age and gender. What's more, risk genes and molecular functions were screened via protein-protein interaction (PPI) network and functional enrichment analysis.</p><p><strong>Results: </strong>Rs118050317 in NINJ2 significantly increased CHD risk in people aged more than 60 years and women. Rs118050317 and rs7307242 had strong relationships with hypertension risk in CHD patients. Additionally, rs75750647 exceedingly raised diabetes risk in cases under multiple models, whereas rs10849390 could protect CHD patients from diabetes in allele, homozygote, and additive models. We also observed two blocks in NINJ2. Further interaction network and enrichment analysis showed that NINJ2 played a greater role in the pathogenesis and progression of CHD.</p><p><strong>Conclusion: </strong>Our results suggest that NINJ2 polymorphisms are associated with CHD risk.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"328-337"},"PeriodicalIF":3.4,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11057668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140183887","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":"Matrin-3 acts as a potential biomarker and promotes hepatocellular carcinoma progression by interacting with cell cycle-regulating genes","authors":"Hengjing He, Muhammad Jamal, Xingruo Zeng, Yufei Lei, Di Xiao, Zimeng Wei, Chengjie Zhang, Xiaoyu Zhang, Shan Pan, Qianshan Ding, Haiyan Tan, Songping Xie, Qiuping Zhang","doi":"10.1080/15384101.2024.2305535","DOIUrl":"https://doi.org/10.1080/15384101.2024.2305535","url":null,"abstract":"Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related mortality worldwide. The oncogenic role of Matrin-3 (MATR3), an a nuclear matrix protein, in HCC remains largely unknow...","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"37 9 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139515703","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}

{"title":"MiR-548t-5p regulates pancreatic ductal adenocarcinoma metastasis through an IL-33-dependent crosstalk between cancer cells and M2 macrophages.","authors":"Yan Wang, Wan-Li Ge, Shao-Jun Wang, Yu-Yong Liu, Zhi-Han Zhang, Yang Hua, Xiong-Fei Zhang, Jing-Jing Zhang","doi":"10.1080/15384101.2024.2309026","DOIUrl":"10.1080/15384101.2024.2309026","url":null,"abstract":"<p><p>IL-33 has been associated with pro- and anticancer functions in cancer. However, its role in pancreatic cancer metastasis remains unknown. This study aimed to explore the role of miR-548t-5p/IL-33 axis in the metastasis of pancreatic cancer. Luciferase activity assay, qRT-PCR, Western blot and ELISA were performed to prove whether IL-33 is the target of miR-548t-5p. In vivo metastasis assay and cellular transwell assay were performed to explore the role of miR-548t-5p/IL-33 axis in the invasion and metastasis of pancreatic cancer. Co-culture experiments and immunohistochemistry were performed to observe whether IL-33 affects cell invasion and metastasis dependent on the involvement of M2 macrophages. THP-1 cell induction experiment and flow cytometry were performed to explore the effect of IL-33 on macrophage polarization. CCK-8, colony formation, cell apoptosis, cell cycle, cell wound healing and transwell assay were performed to investigate the effect of IL-33 induced M2 macrophages on cell malignant biological behavior by coculturing pancreatic cancer cells with the conditioned medium (CM) from macrophages. We found that miR-548t-5p regulated the expression and secretion of IL-33 in pancreatic cancer cells by directly targeting IL-33 mRNA. IL-33 secreted by cancer cells promoted the recruitment and activation of macrophages to a M2-like phenotype. In turn, IL-33 induced M2 macrophages promoted the migration and invasion of cancer cells. Moreover, IL-33 affected pancreatic cancer cell invasion dependent on the involvement of M2 macrophages in the co-culture system. Thus, our study suggested that manipulation of this IL-33-dependent crosstalk has a therapeutic potential for the treatment of pancreatic cancer metastasis.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"169-187"},"PeriodicalIF":3.4,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11037285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139545565","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":"Entero-toxigenic <i>Bacteroides fragilis</i> contributes to intestinal barrier injury and colorectal cancer progression by mediating the BFT/STAT3/ZEB2 pathway.","authors":"Jian Yang, Xue Wang, Tao Hu, He Huang, Gang Chen, Bo Jin, Guilin Zeng, Jian Liu","doi":"10.1080/15384101.2024.2309005","DOIUrl":"10.1080/15384101.2024.2309005","url":null,"abstract":"<p><p>Our previous findings confirmed the high enrichment of <i>Bacteroides fragilis</i> (BF) in fecal samples from patients with colorectal cancer (CRC). The intestinal mucosal barrier is the first defense of the organism against commensal flora and intestinal pathogens and is closely associated with the occurrence and development of CRC. Therefore, this study aimed to investigate the molecular mechanisms through which BF mediates intestinal barrier injury and CRC progression. SW480 cells and a Caco2 intestinal barrier model were treated with entero-toxigenic BF (ETBF), its enterotoxin (B. fragilis toxin, BFT), and non-toxigenic BF (NTBF). Cell counting kit-8, flow cytometry, wound healing and transwell assays were performed to analyze the proliferation, apoptosis, migration, and invasion of SW480 cells. Transmission electron microscopy, FITC-dextran, and transepithelial electrical resistance (TEER) were used to analyze damage in the Caco2 intestinal barrier model. The Azoxymethane/Dextran Sulfate Sodium (AOM/DSS) animal model was established to evaluate the effect of ETBF on intestinal barrier injury and CRC progression <i>in vivo</i>. ETBF and BFT enhanced the viability, wound healing ratio, invasion, and EMT of SW480 cells. In addition, ETBF and BFT disrupted the tight junctions and villus structure in the intestinal barrier model, resulting in increased permeability and reduced TEER. Similarly, the expression of intestinal barrier-related proteins (MUC2, Occludin and Zo-1) was restricted by ETBF and BFT. Interestingly, the STAT3/ZEB2 axis was activated by ETBF and BFT, and treatment with Brevilin A (a STAT3 inhibitor) or knockdown of ZEB2 limited the promotional effect of ETBF and BFT on the SW480 malignant phenotype. <i>In vivo</i> experiments also confirmed that ETBF colonization accelerated tumor load, carcinogenesis, and intestinal mucosal barrier damage in the colorectum of the AOM/DSS animal model, and that treatment with Brevilin A alleviated these processes. ETBF-secreted BFT accelerated intestinal barrier damage and CRC by activating the STAT3/ZEB2 axis. Our findings provide new insights and perspectives for the application of ETBF in CRC treatment.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"70-82"},"PeriodicalIF":4.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11005799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139563628","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":"Small extracellular vesicles promote the formation of the pre-metastatic niche through multiple mechanisms in colorectal cancer.","authors":"Jiyang Wu, Xiaoxing Wang, Zhengzhe Li, Xiaomei Yi, Die Hu, Qi Wang, Tianyu Zhong","doi":"10.1080/15384101.2024.2311501","DOIUrl":"10.1080/15384101.2024.2311501","url":null,"abstract":"<p><p>Colorectal cancer (CRC) ranks among the most prevalent global malignancies, posing significant threats to human life and health due to its high recurrence and metastatic potential. Small extracellular vesicles (sEVs) released by CRC play a pivotal role in the formation of the pre-metastatic niche (PMN) through various mechanisms, preparing the groundwork for accelerated metastatic invasion. This review systematically describes how sEVs promote CRC metastasis by upregulating inflammatory factors, promoting immunosuppression, enhancing angiogenesis and vascular permeability, promoting lymphangiogenesis and lymphatic network remodeling, determining organophilicity, promoting stromal cell activation and remodeling and inducing the epithelial-to-mesenchymal transition (EMT). Furthermore, we explore potential mechanisms by which sEVs contribute to PMN formation in CRC and propose novel insights for CRC diagnosis, treatment, and prognosis.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"131-149"},"PeriodicalIF":4.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11037293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139717328","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":"Integrated analysis of <i>FHIT</i> gene alterations in cancer.","authors":"Lucía Simón-Carrasco, Elena Pietrini, Andrés J López-Contreras","doi":"10.1080/15384101.2024.2304509","DOIUrl":"10.1080/15384101.2024.2304509","url":null,"abstract":"<p><p>The Fragile Histidine Triad Diadenosine Triphosphatase (<i>FHIT</i>) gene is located in the Common Fragile Site FRA3B and encodes an enzyme that hydrolyzes the dinucleotide Ap3A. Although <i>FHIT</i> loss is one of the most frequent copy number alterations in cancer, its relevance for cancer initiation and progression remains unclear. <i>FHIT</i> is frequently lost in cancers from the digestive tract, which is compatible with being a cancer driver event in these tissues. However, <i>FHIT</i> loss could also be a passenger event due to the inherent fragility of the FRA3B locus. Moreover, the physiological relevance of FHIT enzymatic activity and the levels of Ap3A is largely unclear. We have conducted here a systematic pan-cancer analysis of <i>FHIT</i> status in connection with other mutations and phenotypic alterations, and we have critically discussed our findings in connection with the literature to provide an overall view of FHIT implications in cancer.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"92-113"},"PeriodicalIF":4.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11005815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139484640","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}