miR-221-3p对肝癌细胞增殖的影响及相关机制研究

Effect of miR-221-3p on the proliferation of hepatocellular carcinoma cells and related mechanism

目的探讨微小RNA-221-3p(miR-221-3p)对肝癌细胞增殖的影响及其相关机制。方法采用生物学数据库分析肝癌中miR-221-3p的表达水平及其对患者预后的影响。CCK-8、EdU实验分析miR-221-3p对肝癌细胞增殖的影响。采用生物信息学及Western blot探讨miR-221-3p调控肝癌细胞增殖的相关机制。结果miR-221-3p在肝癌中呈高表达,其表达水平与患者总生存率无关。miR-221-3p沉默后肝癌细胞增殖能力减弱,而过表达miR-221-3p后肝癌细胞增殖能力增强。miR-221-3p可以通过负调控残留样蛋白质家族成员4(VGLL4)进而激活JAK2/STAT3信号通路。结论miR-221-3p促进HCC细胞的增殖,其机制可能与负调控VGLL4进而激活JAK2/STAT3信号通路有关。

Objective To explore the effect of microRNA-221-3p(miR-221-3p)on the proliferation of hepatocellular carcinoma(HCC)cells and underlying mechanism.Methods Bioinformatics database were used to analyze the expression of miR-221-3p in hepatocellular carcinoma and its relationship with patient prognosis.The effect of miR-221-3p on the proliferation of HCC cells were analyzed by EdU and CCK-8 assays.Bioinformatics and Western blot were used to investigate the role of miR-221-3p in regulating the proliferation of HCC cells.Results The level of miR-221-3p was up-regulated in HCC,which was not correlated with overall survival.The proliferation of HCC cells was attenuated by miR-221-3p silencing but enhanced by miR-221-3p overexpression.MiR-221-3p activated the JAK2/STAT3 signaling pathway through negatively regulating vestigial-like family member 4(VGLL4).Conclusions Mir-221-3p can promote the proliferation of HCC cells,which may be related to its negative regulatory effect on VGLL4 and further activation of the JAK2/STAT3 signaling pathway.