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miR-557 suppresses hepatocellular carcinoma cell proliferation and migration via downregulating CBX4
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作者 XULONG SUN wentao ding +1 位作者 CHAO JIANG ZHIAN FANG 《BIOCELL》 SCIE 2024年第7期1071-1079,共9页
Introduction:Hepatocellular carcinoma(HCC),a prevalent malignancy,poses significant challenges with high tumor heterogeneity and poor prognosis.MicroRNAs(miRNAs)play a pivotal role in hepatocarcinogenesis.Although abno... Introduction:Hepatocellular carcinoma(HCC),a prevalent malignancy,poses significant challenges with high tumor heterogeneity and poor prognosis.MicroRNAs(miRNAs)play a pivotal role in hepatocarcinogenesis.Although abnormalities in microRNA-557(miR-557)expression have been implicated in various cancer types,its role in HCC remains unclear.Therefore,there is a need to explore the function of microRNA-557 in HCC.Methods:Candidate miRNAs were identified through screening in GSE108724 and GSE20077.Real-time PCR was employed to analyze the expression level of miR-557 in hepatoma cell lines and tissues.Cell viability and migration assays were applied to assess the impact of miR-557 on HCC cell lines.Furthermore,the miR-557 target was predicted through three algorithms(Targetscan,miRWalk,and miRanda),and this was confirmed through luciferase assay and Western blotting.Results:In this study,miR-557 was identified in two datasets and expressed at a low level in both hepatoma cell lines and tissues.Notably,high expression of miR-557 in HCC cells inhibited oncogenesis.Conversely,low expression of miR-557 enhanced tumor proliferation and migration.Polycomb chromobox 4(CBX4)was identified as a direct target of miR-557.Silencing CBX4 influenced the functional impact of miR-557 on HCC cell migration.Conclusion:Taken together,our study contributed to elucidating the hepatoma molecular heterogeneity and provided novel insights into miR-557 role and its target CBX4 in HCC,suggesting its potential as a future effectively druggable target for HCC intervention. 展开更多
关键词 Hepatocellular carcinoma miR-557 Chromobox 4 HEPATOCARCINOGENESIS
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