MiR‐490‐5p inhibits the stemness of hepatocellular carcinoma cells by targeting ECT2

• DOI: 10.1002/jcb.27459
• Publication Date: 2018-09-12T06:53:18Z
• Authors: Yuanjie Yu; Ou Cai; Pengbo Wu; Shiyun Tan
• Keywords: Male; 0303 health sciences; Binding Sites; Carcinoma, Hepatocellular; Cell Survival; Liver Neoplasms; Hep G2 Cells; Middle Aged; Prognosis; Disease-Free Survival; 3. Good health; Gene Expression Regulation, Neoplastic; MicroRNAs; 03 medical and health sciences; Hyaluronan Receptors; Ki-67 Antigen; Proto-Oncogene Proteins; Humans; Female; AC133 Antigen; 3' Untranslated Regions; Aged; Cell Proliferation

Abstract To explore the targeting relationship between miR‐490‐5p and ECT2 in hepatocellular carcinoma (HCC) influences of on stemness HCC cells. The expressions tissues adjacent were identified by quantitative real‐time polymerase chain reaction (qRT‐PCR). relationships expression levels miR‐490‐5p/ overall/disease‐free survival (OS/DFS) patients with evaluated using correlative curves. In addition, was predicted TargetScan verified dual‐luciferase reporter assay. Plasmid transfection used for overexpression HepG2 cells, efficiency qRT‐PCR. Cell Counting Kit‐8 assay cell sphere‐formation conducted to detect proliferation ability respectively. populations different transfections sorted flow cytometry. proteins stem signaling pathway determined Western blot analysis. MiR‐490‐5p remarkably downregulated, yet upregulated compared tissues. positively correlated OS DFS HCC, which otherwise negatively expression. validated be downstream target miR‐490‐5p. Overexpression restrained sphere formation ability, stemness, repressed cells through inhibiting . may an underlying therapeutic treatment.