Cell Cycle最新文献_第7页

The sorafenib resistance-related gene signature predicts prognosis and indicates immune activity in hepatocellular carcinoma. 索拉非尼耐药相关基因特征可预测预后并显示肝细胞癌的免疫活性。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-01-01 Epub Date: 2024-03-05 DOI: 10.1080/15384101.2024.2309020

Tianxin Luo, Xiaomei Chen, Wei Pan, Shu Zhang, Jian Huang

{"title":"The sorafenib resistance-related gene signature predicts prognosis and indicates immune activity in hepatocellular carcinoma.","authors":"Tianxin Luo, Xiaomei Chen, Wei Pan, Shu Zhang, Jian Huang","doi":"10.1080/15384101.2024.2309020","DOIUrl":"10.1080/15384101.2024.2309020","url":null,"abstract":"Hepatocellular carcinoma (HCC) is the second most common cause of cancer-related death worldwide. Most patients with advanced HCC acquire sorafenib resistance. Drug resistance reflects the heterogeneity of tumors and is the main cause of tumor recurrence and death.We identified and validated sorafenib resistance related-genes (SRGs) as prognostic biomarkers for HCC. We obtained SRGs from the Gene Expression Omnibus and selected four key SRGs using the least absolute shrinkage and selection operator, random forest, and Support Vector Machine-Recursive feature elimination machine learning algorithms. Samples from the The Cancer Genome Atlas (TCGA)-HCC were segregated into two groups by consensus clustering. Following difference analysis, 19 SRGs were obtained through univariate Cox regression analysis, and a sorafenib resistance model was constructed for risk stratification and prognosis prediction. In multivariate Cox regression analysis, the risk score was an independent predictor of overall survival (OS). Patients classified as high-risk were more sensitive to other chemotherapy drugs and showed a higher expression of the common immune checkpoints. Additionally, the expression of drug-resistance genes was verified in the International Cancer Genome Consortium cohort. A nomogram model with a risk score was established, and its prediction performance was verified by calibration chart analysis of the TCGA-HCC cohort. We conclude that there is a significant correlation between sorafenib resistance and the tumor immune microenvironment in HCC. The risk score could be used to identify a reliable prognostic biomarker to optimize the therapeutic benefits of chemotherapy and immunotherapy, which can be helpful in the clinical decision-making for HCC patients.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"150-168"},"PeriodicalIF":3.4,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11037289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140038821","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

TOP3A coupling with replication forks and repair of TOP3A cleavage complexes. TOP3A 与复制叉的耦合以及 TOP3A 裂解复合物的修复。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-01-01 Epub Date: 2024-02-11 DOI: 10.1080/15384101.2024.2314440

Liton Kumar Saha, Yves Pommier

引用次数: 0

ZC3H12A inhibits tumor growth and metastasis of breast cancer under hypoxic condition via the inactivation of IL-17 signaling pathway. ZC3H12A 通过抑制 IL-17 信号通路，抑制缺氧条件下乳腺癌的生长和转移。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-01-01 Epub Date: 2024-02-15 DOI: 10.1080/15384101.2024.2314441

Zhongbing Luo, Fulan Yang, Kang Liu, Zhenluo Ding

{"title":"ZC3H12A inhibits tumor growth and metastasis of breast cancer under hypoxic condition via the inactivation of IL-17 signaling pathway.","authors":"Zhongbing Luo, Fulan Yang, Kang Liu, Zhenluo Ding","doi":"10.1080/15384101.2024.2314441","DOIUrl":"10.1080/15384101.2024.2314441","url":null,"abstract":"Hypoxia is a major contributor to tumor microenvironment (TME) and metastasis in most solid tumors. We seek to screen hypoxia-related genes affecting metastasis in breast cancer and to reveal relative potential regulatory pathway. Based on gene expression profiling of GSE17188 dataset, differential expressed genes (DEGs) were identified between highly metastatic breast cancer cells under hypoxia and samples under normoxia. The protein-protein interaction (PPI) network was utilized to determine hub genes. The gene expression profiling interactive analysis database (GEPIA2) and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were employed to quantify hub genes. Moreover, overexpression of zinc finger CCCH-type containing 12A (ZC3H12A) was performed both in breast cancer cells and xenograft mouse model to determine the role of ZC3H12A. We identified 134 DEGs between hypoxic and normoxic samples. Based on PPI analysis, 5 hub genes interleukin (IL)-6, GALN (GAL), CD22 molecule (CD22), ZC3H12A and TNF receptor associated factor 1 (TRAF1) were determined; the expression levels of TRAF1, IL-6, ZC3H12A and GAL were remarkably downregulated while CD22 was upregulated in breast cancer cells. Besides, patients with higher expression of ZC3H12A had favorable prognosis. Overexpression of ZC3H12A could inhibit metastasis and tumor growth of breast cancer; overexpression of ZC3H12A downregulated the expression of IL-17 signaling pathway-related proteins such as IL-17 receptor A (IL-17RA), IL-17A and nuclear factor κB activator 1 (Act1). This study reveals ZC3H12A and IL-17 signaling pathway as potential therapeutic targets for hypoxic breast cancer.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"188-204"},"PeriodicalIF":3.4,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11037279/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139734605","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

Impact of sunitinib resistance on clear cell renal cell carcinoma therapeutic sensitivity in vitro. 舒尼替尼耐药性对透明细胞肾细胞癌体外治疗敏感性的影响

IF 4.3 3区生物学

Cell Cycle Pub Date : 2024-01-01 Epub Date: 2024-01-23 DOI: 10.1080/15384101.2024.2306760

Susmita Ghosh, Mamatha Garige, Patrick R Haggerty, Alexis Norris, Chao-Kai Chou, Wells W Wu, Rong-Fong Shen, Carole Sourbier

{"title":"Impact of sunitinib resistance on clear cell renal cell carcinoma therapeutic sensitivity in vitro.","authors":"Susmita Ghosh, Mamatha Garige, Patrick R Haggerty, Alexis Norris, Chao-Kai Chou, Wells W Wu, Rong-Fong Shen, Carole Sourbier","doi":"10.1080/15384101.2024.2306760","DOIUrl":"10.1080/15384101.2024.2306760","url":null,"abstract":"Sunitinib resistance creates a major clinical challenge for the treatment of advanced clear cell renal cell carcinoma (ccRCC) and functional and metabolic changes linked to sunitinib resistance are not fully understood. We sought to characterize the molecular and metabolic changes induced by the development of sunitinib resistance in ccRCC by developing and characterizing two human ccRCC cell lines resistant to sunitinib. Consistent with the literature, sunitinib-resistant ccRCC cell lines presented an aberrant overexpression of Axl and PD-L1, as well as a metabolic rewiring characterized by enhanced OXPHOS and glutamine metabolism. Therapeutic challenges of sunitinib-resistant ccRCC cell lines in vitro using small molecule inhibitors targeting Axl, AMPK and p38, as well as using PD-L1 blocking therapeutic antibodies, showed limited CTL-mediated cytotoxicity in a co-culture model. However, the AMPK activator metformin appears to sensitize the effect of PD-L1 blocking therapeutic antibodies and to enhance CTLs' cytotoxic effects on ccRCC cells. These effects were not broadly observed with the Axl and the p38 inhibitors. Taken together, these data suggest that targeting certain pathways aberrantly activated by sunitinib resistance such as the AMPK/PDL1 axis might sensitize ccRCC to immunotherapies as a second-line therapeutic approach.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"43-55"},"PeriodicalIF":4.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11005810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139541942","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

Dehydroandrographolide alleviates rheumatoid arthritis by inhibiting neutrophil activation via LMIR3 in collagen induced arthritis rats. 脱氢穿心莲内酯通过LMIR3抑制胶原诱导的关节炎大鼠中性粒细胞的活化，从而缓解类风湿性关节炎。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-01-01 Epub Date: 2024-01-17 DOI: 10.1080/15384101.2024.2304508

Ning Kong, Huanshuai Guan, Xudong Duan, Ruomu Cao, Heng Li, Fangze Xing, Xueshan Du, Yi Zheng, Lei Zhang, Yiyang Li, Zeyu Liu, Run Tian, Kunzheng Wang, Delu Che, Pei Yang

{"title":"Dehydroandrographolide alleviates rheumatoid arthritis by inhibiting neutrophil activation via LMIR3 in collagen induced arthritis rats.","authors":"Ning Kong, Huanshuai Guan, Xudong Duan, Ruomu Cao, Heng Li, Fangze Xing, Xueshan Du, Yi Zheng, Lei Zhang, Yiyang Li, Zeyu Liu, Run Tian, Kunzheng Wang, Delu Che, Pei Yang","doi":"10.1080/15384101.2024.2304508","DOIUrl":"10.1080/15384101.2024.2304508","url":null,"abstract":"Rheumatoid arthritis (RA) is an inflammatory disease which causes severe pain and disability. Neutrophils play essential roles in the onset and progression of RA; thus, inhibition of neutrophil activation is becoming a popular therapeutic strategy. Dehydroandrographolide has provided satisfactory outcomes in inflammatory diseases; however, its therapeutic effects and mechanism in RA are not fully understood. Leukocyte mono-immunoglobulin-like receptor 3 (LMIR3) is a negative regulator highly expressed in neutrophils. To determine whether dehydroandrographolide negatively regulated neutrophils activation via LMIR3, cytokines release and collagen-induced arthritis (CIA) rats were used in vitro and in vivo. Biacore, molecular docking analysis and molecular dynamics simulation were performed to prove the target of dehydroandrographolide. Moreover, the downstream signaling pathways of LMIR3 activation were analyzed by western blotting. Results showed that oral dehydroandrographolide administration of 2 mg/kg/day to CIA rats attenuated synovitis and bone and cartilage damage after the 28-day intervention, revealed using HE sections and micro-CT. Dehydroandrographolide significantly inhibited cytokine release and chemotaxis of LPS/TNF-α-activated neutrophils in vitro. Dehydroandrographolide inhibited neutrophils activation via binding to LMIR3. Moreover, dehydroandrographolide up-regulated the phosphorylation of SHP-1 and SHP-2, which are the essential kinases in the LMIR3 signaling pathways. This study revealed that dehydroandrographolide attenuated collagen-induced arthritis by suppressing neutrophil activation via LMIR3.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-14"},"PeriodicalIF":3.4,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11005808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139484629","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

YAP1 expression in colorectal cancer confers the aggressive phenotypes via its target genes. YAP1 在结直肠癌中的表达通过其靶基因赋予侵袭性表型。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-01-01 Epub Date: 2024-01-23 DOI: 10.1080/15384101.2024.2309017

Haoyuan Chen, Yangyang Shang, Xia Li, Rongquan Wang

{"title":"YAP1 expression in colorectal cancer confers the aggressive phenotypes via its target genes.","authors":"Haoyuan Chen, Yangyang Shang, Xia Li, Rongquan Wang","doi":"10.1080/15384101.2024.2309017","DOIUrl":"10.1080/15384101.2024.2309017","url":null,"abstract":"Yes-associated protein1 (YAP1), a downstream effector of the Hippo pathway, is over-expressed in several types of malignancies. We analyzed retrospectively the TCGA database using 447 colorectal cancer (CRC) samples to determine the correlation between YAP1 expression level and CRC patient prognosis. YAP1-enforced expressed CRC cell lines were constructed using the lentivirus particles containing a YAP1 insert. YAP1 was highly expressed in CRC cancerous tissues and is associated with distant metastasis of CRC patients. Kaplan - Meier analysis indicated that CRC patients with a higher YAP1 expression group (n = 104) had worse disease-free survival (DFS) and overall survival (OS) than lower YAP1 expression group (n = 343) (p = 0.008 and p = 0.022). Univariate and multivariate analysis indicated that the elevated YAP1 expression predicted the aggressive phenotype and was an independent indicator for OS and DFS of CRC patients. YAP1 over-expression in CRC cells enhanced their migration and invasion significantly which can be reversed by AXL, CTGF, or CYR61 interference. The study suggested that YAP1 affected the prognosis of CRC patients and controlled the abilities of invasion and migration of CRC cells via its target genes AXL, CTGF, and CYR61.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"83-91"},"PeriodicalIF":3.4,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11005797/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139541964","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

Correction. 更正。

IF 4.3 3区生物学

Cell Cycle Pub Date : 2024-01-01 Epub Date: 2024-02-13 DOI: 10.1080/15384101.2024.2312745

引用次数: 0

Sirt6 promotes DNA damage repair in osteoarthritis chondrocytes by activating the Keap1/Nrf2/HO-1 signaling pathway. Sirt6通过激活Keap1/Nrf2/HO-1信号通路促进骨关节炎软骨细胞的DNA损伤修复。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-01-01 Epub Date: 2024-02-22 DOI: 10.1080/15384101.2024.2316493

Ling-Wei Mao, Qin-Yi Jiang, Nan Meng, Li Xiao, Qi Zhang, Yong-Xin Chen, Lin-Juan Liu, Lei Wang

{"title":"Sirt6 promotes DNA damage repair in osteoarthritis chondrocytes by activating the Keap1/Nrf2/HO-1 signaling pathway.","authors":"Ling-Wei Mao, Qin-Yi Jiang, Nan Meng, Li Xiao, Qi Zhang, Yong-Xin Chen, Lin-Juan Liu, Lei Wang","doi":"10.1080/15384101.2024.2316493","DOIUrl":"10.1080/15384101.2024.2316493","url":null,"abstract":"The aim of this study was to explore the effect and mechanism of Sirt6 on DNA damage repair in OA chondrocytes. Cartilage tissues were collected from OA patients with knee arthroplasty and traumatic amputation patients without OA. Besides, 7-week-old male C57BL/6 mice were randomly divided into Control and OA groups; CHON-001 cells of corresponding groups were treated with 10 ng/ml interleukin (IL)-1β, respectively. Subsequently, Sirt6 or siNrf2 was over-expressed in CHON-001 cells to observe the effect of Sirt6 on DNA damage and senescence of chondrocytes by IL-1β through the nuclear factor E2-related factor 2 (Nrf2) signaling pathway. The expression level of Sirt6 in human and mouse OA cartilage tissues was significantly decreased. However, 24 h of treatment with IL-1β significantly decreased the expression of Sirt6 in chondrocytes, induced DNA damage, and promoted cellular senescence. In addition, over-expression of Sirt6 promoted DNA damage repair and inhibited cellular senescence in IL-1β-induced chondrocytes. Moreover, the overexpression of Sirt6 activated the Keap1/Nrf2/HO-1 signaling pathway in chondrocytes, while knockdown of Nrf2 expression inhibited the DNA damage repair and anti-senescence effects of Sirt6 on IL-1β-treated chondrocytes. Sirt6 may reduce DNA damage and cellular senescence in OA chondrocytes induced by IL-1β through activating the Keap1/Nrf2/HO-1 signaling pathway.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"205-217"},"PeriodicalIF":3.4,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11037281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139930229","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

B-cell ALL with SOX11 gene amplification associates with a worse outcome. SOX11基因扩增的B细胞ALL预后较差。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-01-01 Epub Date: 2024-02-13 DOI: 10.1080/15384101.2024.2306756

George Angelakakis, Mallika Varkhedi, Toriana R Dabkowski, Michael J Diaz, Michelle Yeagley, George Blanck

引用次数: 0

ARRDC3 regulates the targeted therapy sensitivity of clear cell renal cell carcinoma by promoting AXL degradation. ARRDC3通过促进AXL降解调节透明细胞肾细胞癌的靶向治疗敏感性。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-01-01 Epub Date: 2024-02-22 DOI: 10.1080/15384101.2024.2308411

Mulin Chen, Bingde Yin, Yao Liu, Mingzi Li, Suqin Shen, Jiaxue Wu, Weiguo Li, Jie Fan

{"title":"ARRDC3 regulates the targeted therapy sensitivity of clear cell renal cell carcinoma by promoting AXL degradation.","authors":"Mulin Chen, Bingde Yin, Yao Liu, Mingzi Li, Suqin Shen, Jiaxue Wu, Weiguo Li, Jie Fan","doi":"10.1080/15384101.2024.2308411","DOIUrl":"10.1080/15384101.2024.2308411","url":null,"abstract":"AXL plays crucial roles in the tumorigenesis, progression, and drug resistance of neoplasms; however, the mechanisms associated with AXL overexpression in tumors remain largely unknown. In this study, to investigate these molecular mechanisms, wildtype and mutant proteins of arrestin domain-containing protein 3 (ARRDC3) and AXL were expressed, and co-immunoprecipitation analyses were performed. ARRDC3-deficient cells generated using the CRISPR-Cas9 system were treated with different concentrations of the tyrosine kinase inhibitor sunitinib and subjected to cell biological, molecular, and pharmacological experiments. Furthermore, immunohistochemistry was used to analyze the correlation between ARRDC3 and AXL protein expressions in renal cancer tissue specimens. The experimental results demonstrated that ARRDC3 interacts with AXL to promote AXL ubiquitination and degradation, followed by the negative regulation of downstream signaling mechanisms, including the phosphorylation of protein kinase B and extracellular signal-regulated kinase. Notably, ARRDC3 deficiency decreased the sunitinib sensitivity of clear cell renal cell carcinoma (ccRCC) cells in a manner dependent on the regulation of AXL stability. Overall, our results suggest that ARRDC3 is a negative regulator of AXL and can serve as a novel predictor of sunitinib therapeutic response in patients with ccRCC.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"56-69"},"PeriodicalIF":3.4,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11005801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139930228","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