Coxsackievirus A6 Induces Cell Cycle Arrest in G0/G1 Phase for Viral Production

Wang, Zengyan; Wang, Yue; Wang, Shaohua; Meng, Xiang-Ling; Song, Fang; Huo, Wenbo; Zhang, Shuxia; Chang, Junliang; Li, Jingliang; Zheng, Baisong; Li, Yanqiu; Zhang, Yahong; Zhang, Wenyan; Yu, Jinghua

doi:10.3389/fcimb.2018.00279

Cited by 43 publications

(38 citation statements)

References 45 publications

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“…cyclins are widely distributed in eukaryotic cells and, among them, ccnd1, encoding cyclin d1, is a highly conserved cell cycle family protein (15,16). Through responding to growth factor signaling, cyclin d1 promotes the cell cycle transition from the G1 to S phase, thus regulating cell cycle progression (17)(18)(19). In addition, having been identified as a proto-oncogene, the abnormal expression of cyclin d1 promotes cell colonization through regulating the cell cycle and arresting cells during synthesis (20).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

Guo

Xue

2020

Mol Med Report

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Microrna (mir)-628-5p serves as an antitumor gene in a variety of cancers; however, the role of mir-628-5p in colorectal cancer remains largely unclear. The purpose of this study was to investigate the role and mechanism of mir-628-5p in colorectal cancer. reverse transcription-quantitative Pcr (RT-qPCR), colony formation assays and flow cytometric analysis were used to determine the expression levels of mir-628-5p in colorectal cancer tissues and cell lines, and the proliferative ability of colorectal cancer cells. TargetScan version 7.2 and dual-luciferase reporter assay were performed to predict and confirm mir-628-5p target genes. The expression levels of cyclin d1 (ccnd1) and related genes were determined using rT-qPcr or/and western blotting analysis. mir-628-5p mimics and ccnd1 plasmids were used to overexpress mir-628-5p and ccnd1; it was demonstrated that the expression levels of miR-628-5p were significantly downregulated in colorectal cancer tissues and cell lines. mir-628-5p mimic-transfected cells inhibited the proliferation and induced apoptosis of HT-29 cells. ccnd1, a downstream effector of mir-628-5p, promoted the proliferation and suppressed apoptosis of HT-29 cells, and the effects were reversed by mir-628-5p mimics. in conclusion, the present study suggested that colorectal cancer progression may be regulated through the mir-628-5p/ccnd1 axis, and mir-628-5p could be used as a potential diagnostic and prognostic biomarker for colorectal cancer.

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Section: Introductionmentioning

confidence: 99%

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

Guo

Xue

2020

Mol Med Report

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“…By exploring how SARS-CoV-2 nsp1 controls host cells, we confirm that although SARS-CoV-2 nsp1 has no toxic effect, it promotes host-cell retention in G0/G1 phase. Many viruses, such as Coxsackievirus A6 and Murine norovirus-1, can induce cell-cycle arrest in G0/G1 phase [51,52], providing a favourable environment for viral production. Furthermore, the viral non-structural protein 3D of Enterovirus D68 (EV-D68) are demonstrated to be responsible for the G0/G1 phase arrest prevents, which can promote viral production [53].…”

Section: Discussionmentioning

confidence: 99%

Lysine 164 is critical for SARS-CoV-2 Nsp1 inhibition of host gene expression

Shen

Zhang

Yang

et al. 2021

Journal of General Virology

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The emerging pathogen severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused social and economic disruption worldwide, infecting over 9.0 million people and killing over 469 000 by 24 June 2020. Unfortunately, no vaccine or antiviral drug that completely eliminates the transmissible disease coronavirus disease 2019 (COVID-19) has been developed to date. Given that coronavirus nonstructural protein 1 (nsp1) is a good target for attenuated vaccines, it is of great significance to explore the detailed characteristics of SARS-CoV-2 nsp1. Here, we first confirmed that SARS-CoV-2 nsp1 had a conserved function similar to that of SARS-CoV nsp1 in inhibiting host-protein synthesis and showed greater inhibition efficiency, as revealed by ribopuromycylation and Renilla luciferase (Rluc) reporter assays. Specifically, bioinformatics and biochemical experiments showed that by interacting with 40S ribosomal subunit, the lysine located at amino acid 164 (K164) was the key residue that enabled SARS-CoV-2 nsp1 to suppress host gene expression. Furthermore, as an inhibitor of host-protein expression, SARS-CoV-2 nsp1 contributed to cell-cycle arrest in G0/G1 phase, which might provide a favourable environment for virus production. Taken together, this research uncovered the detailed mechanism by which SARS-CoV-2 nsp1 K164 inhibited host gene expression, laying the foundation for the development of attenuated vaccines based on nsp1 modification.

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“…CCND1, also known as cyclin D1, is a member of the cell cycle family of proteins [26]. CCND1 regulates cell cycle progression by promoting the cell cycle transition from G1 to S phase [27][28][29]. The abnormal expression of CCND1 promotes cell proliferation by regulating the cell cycle [30].…”

Section: Discussionmentioning

confidence: 99%

Bioinformatic analysis reveals MIR502 as a potential tumour suppressor in ovarian cancer

et al. 2020

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Background: Ovarian cancer (OC) is a major cause of death among women due to the lack of early screening methods and its complex pathological progression. Increasing evidence has indicated that microRNAs regulate gene expression in tumours by interacting with mRNAs. Although the research regarding OC and microRNAs is extensive, the vital role of MIR502 in OC remains unclear. Methods: We integrated two microRNA expression arrays from GEO to identify differentially expressed genes. The Kaplan-Meier method was used to screen for miRNAs that had an influence on survival outcome. Upstream regulators of MIR502 were predicted by JASPAR and verified by ChIP-seq data. The LinkedOmics database was used to study genes that were correlated with MIR502. Gene Set Enrichment Analysis (GSEA) was conducted for functional annotation with GO and KEGG pathway enrichment analyses by using the open access WebGestalt tool. We constructed a PPI network by using STRING to further explore the core proteins. Results: We found that the expression level of MIR502 was significantly downregulated in OC, which was related to poor overall survival. NRF1, as an upstream regulator of MIR502, was predicted by JASPAR and verified by ChIP-seq data. In addition, anti-apoptosis and pro-proliferation genes in the Hippo signalling pathway, including CCND1, MYC, FGF1 and GLI2, were negatively regulated by MIR502, as shown in the GO and KEGG pathway enrichment results. The PPI network further demonstrated that CCND1 and MYCN were at core positions in the development of ovarian cancer. Conclusions: MIR502, which is regulated by NRF1, acts as a tumour suppressor gene to accelerate apoptosis and suppress proliferation by targeting the Hippo signalling pathway in ovarian cancer.

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Coxsackievirus A6 Induces Cell Cycle Arrest in G0/G1 Phase for Viral Production

Cited by 43 publications

References 45 publications

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

Lysine 164 is critical for SARS-CoV-2 Nsp1 inhibition of host gene expression

Bioinformatic analysis reveals MIR502 as a potential tumour suppressor in ovarian cancer

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