MicroRNA‑363‑3p inhibits hepatocarcinogenesis by targeting HMGA2 and is associated with liver cancer stage.

Abstract

The importance of microRNAs (miRNAs) in cancer development has been widely recognized in recent decades. In the present study, the function and mechanism of miRNA-363-3p (miR-363-3p), formerly characterized as a tumor suppressor, in the hepatocarcinogenesis of liver cancer cells was investigated. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was applied to detect the expression of miR-363-3p in liver cancer tissues. Cell proliferation, survival and migration capacities were determined by MTT, colony formation and wound-healing assays, respectively. The targeting of high mobility group AT-hook 2 (HMGA2) mRNA by miR-363-3p was confirmed by bioinformatics analysis, and RT-qPCR, luciferase reporter and western blot assays. The correlation between the expression levels of HMGA2 and miR-363-3p was analyzed. The RT-qPCR results revealed that the levels of miR-363-3p were downregulated in liver cancer tissues. Cellular assays validated that miR-363-3p exerted tumor suppressing functions, including the inhibition of cell proliferation, survival and migration abilities in two liver cancer cell lines. Bioinformatics prediction and subsequent experiments demonstrated that HMGA2 was a direct target of miR-363-3p. Restoration of the expression of HMGA2 in miR-363-3p mimic-transfected cells reversed the tumor suppressing effects caused by miR-363-3p. Finally, there was a significant negative correlation between the expression levels of HMGA2 and miR-363-3p in liver cancer tissues. miR-363-3p was identified as an important tumor suppressor in liver cancer via targeting HMGA2, which may have potential benefits in liver cancer therapy.