The Novel Action of miR-193b-3p/CDK1 Signaling in HCC Proliferation and Migration: A Study Based on Bioinformatic Analysis and Experimental Investigation.

Abstract

Hepatocellular carcinoma (HCC) is a common human malignancy with high mortality and dismal prognosis. A growing number of novel targets underlying HCC pathophysiology have been detected using microarray high throughput screening platforms. This study carried out bioinformatics analysis to explore underlying biomarkers in HCC and assessed the potential action of the miR-193b-3p/CDK1 signaling pathway in HCC progression. A total of 241 common differentially expressed genes (DEGs) were screened from GSE33294, GSE104310, and GSE144269. Functional analysis results implicated that DEGs are significantly associated with "cell cycle," "cell division," and "proliferation." The protein-protein interaction network analysis extracted ten hub genes from common DEGs. Ten hub genes were significantly overexpression in HCC tissues. Kaplan-Meier survival analysis revealed that 10 hub genes were linked with a poorer prognosis in HCC patients. Functional assays showed that CDK1 knockdown repressed HCC cell proliferation and migration. Luciferase reporter assay showed that miR-193b-3p could target CDK1 3' untranslated region, and miR-193b-3p negatively modulated CDK1. Enforced CDK1 expression attenuated miR-193b-3p-modulated suppressive actions on HCC cell proliferation and migration. To summarize, we performed a comprehensive bioinformatics analysis and identified 10 hub genes linked to the prognosis in HCC patients. Functional analysis revealed that CDK1, negatively regulated by miR-193b-3p, may act as an oncogene to promote HCC cell proliferation and migration and may predict poor prognosis of HCC patients. However, the role of CDK1/miR-193b-3p may still require further investigation.