Abstract
ObjectiveThis study aims to explore the mechanism of the miR-424-5p/E2F7 axis in hepatocellular carcinoma (HCC) and provide new ideas for targeted therapy of HCC.MethodsBioinformatics analysis was used to identify the target differentially expressed miRNA in HCC and predict its target gene. qRT-PCR was employed to verify the expression of miR-424-5p and E2F7 mRNA in HCC cells. Western blot was performed to detect the effect of miR-424-5p ectopic expression on the protein expression of E2F7. CCK-8 was used to detect proliferative activity of HCC cells and flow cytometry was carried out for analyzing cell cycle distribution. Dual luciferase reporter assay was conducted to verify the direct targeting relationship between miR-424-5p and E2F7.ResultsWe observed that miR-424-5p was down-regulated in HCC cells. CCK-8 showed that overexpression of miR-424-5p inhibited cell proliferation, and flow cytometry showed that miR-424-5p could block cells in G0/G1 phase. E2F7 was up-regulated in HCC cells, and E2F7 overexpression could facilitate the proliferative ability of HCC cells and promote the cell cycle progressing from G0/G1 to S phase. Furthermore, dual-luciferase reporter assay indicated that miR-424-5p could directly down-regulate E2F7 expression. Analysis on cell function demonstrated that miR-424-5p inhibited the proliferation of HCC cells and blocked cell cycle at G0/G1 phase by targeting E2F7.ConclusionOur results proved that E2F7 was a direct target of miR-424-5p, and miR-424-5p could regulate cell cycle and further inhibit the proliferation of HCC cells by targeting E2F7.
Highlights
The mortality rate of hepatocellular carcinoma (HCC) ranks the third among malignant tumors in the world, with about 1 million new cases diagnosed each year, and the incidence rate of HCC continues to rise [1,2]
cell counting kit 8 (CCK-8) showed that overexpression of miR-424-5p inhibited cell proliferation, and flow cytometry showed that miR424-5p could block cells in G0/G1 phase
E2F7 was up-regulated in HCC cells, and E2F7 overexpression could facilitate the proliferative ability of HCC cells and promote the cell cycle progressing from G0/G1 to S phase
Summary
The mortality rate of hepatocellular carcinoma (HCC) ranks the third among malignant tumors in the world, with about 1 million new cases diagnosed each year, and the incidence rate of HCC continues to rise [1,2]. Many studies have reported the abnormal expression and biological function of miRNAs in liver cancer. MiR-486 is obviously down-regulated in liver cancer, and its ectopic expression can hinder the occurrence of tumor [10]. MiR-498 inhibits growth and metastasis of liver cancer by targeting and down-regulating the expression of ZEB2 [11]. Recent studies have shown that miR-424-5p is down-regulated in cancers including intrahepatic cholangiocarcinoma, esophageal squamous cell carcinoma and epithelial ovarian cancer [14,15,16], and inhibits proliferation and metastasis of cancer cells. The underlying molecular mechanism and the specific biological function of miR-424-5p in HCC have not been fully elucidated. Studying the mechanism of miR-424-5p in HCC is beneficial for the development of new strategies for the prognosis and treatment of HCC
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