MiR-1297 promotes apoptosis and inhibits the proliferation and invasion of hepatocellular carcinoma cells by targeting HMGA2.

Abstract

MicroRNAs (miRNAs) have recently emerged as important regulators of gene expression in various tissues. In particular, miRNAs have been identified as new therapeutic agents and biomarkers in cancer. The aim of the present study was to explore whether miR‑1297 has an anti‑cancer role in hepatocellular carcinoma cell lines and to explore its underlying mechanism. The proliferation, apoptosis and migration of hepatocellular carcinoma cells were evaluated by cell viability assay, TUNEL staining and a wound healing assay, respectively. Western blot analysis and reverse transcription polymerase chain reaction (RT‑PCR) were performed to determine the expression levels of proteins and mRNAs of high‑mobility group AT‑hook 2 (HMGA2) in hepatocellular carcinoma. The luciferase assay was employed to verify the inhibitory activity of miR‑1297 on the 3' untranslated region (3'UTR) of the HMGA2 gene. In the present study, overexpression of miR‑1297 significantly inhibited the proliferation of HepG2 and SMMC7721 cells. Forced expression of miR‑1297 also increased the apoptosis of HepG2 and SMMC7721. Furthermore, the migration of HepG2 and SMMC7721 was also clearly suppressed by miR‑1297 overexpression. All these effects can be abrogated by co‑transfection with miR‑1297 inhibitor‑AMO‑1297. The luciferase assay verified that miR‑1297 overexpression is able to inhibit the activity of luciferase reporter harboring the HMGA2 3'UTR, indicating HMGA2 as the target of miR‑1297. Although the HMGA2 level was not affected by miR‑1297, the HMGA2 protein was significantly inhibited by miR‑1297 overexpression. Collectively, miR‑1297 was revealed to regulate the proliferation, apoptosis and migration of hepatocellular carcinoma cells via acting on HMGA2. The finding provides a new target for the treatment of hepatocellular carcinoma.