miR-34a regulates HDAC1 expression to affect the proliferation and apoptosis of hepatocellular carcinoma.

作者：Tingyi Sun, Hongjian Xie, Zhen Li, Lingfei Kong, Xiang-Nan Gou, Du-Juan Li, Yujie Shi, Yan-Zhi Ding · 发表于：PubMed · 年份：2017 · 被引用次数：51 · 研究领域：MicroRNA in disease regulation、Cancer-related molecular mechanisms research、Circular RNAs in diseases

<0.05). In addition, miR-34a expression was negatively related to HDAC1 expression. miR-34a mimic was transfected into HCC cell lines (HepB3 and HepG2). CCK8 assay, colony formation assay and flow cytometry showed miR-34a over-expression could inhibit the proliferation of HCC cells and induce their apoptosis. Western blotting indicated miR-34a over-expression down-regulated the expression of Bcl-2, procaspase-3, procaspase-9 and c-Myc, but up-regulate p21 expression. Bioinformatics analysis indicated HDAC1 was a target gene of miR-34a. Dual Luciferase Reporter Gene Assay and retrieval assay showed miR-34a could act at the 3'UTR of HDAC1 gene to regulate its expression. Thus, miR-34a may inhibit the proliferation of HCC cells and induce their apoptosis via regulating HDAC1 expression. Our findings provide evidence for the diagnosis and therapeutic target of HCC.