miR-760 mediated the proliferation and metastasis of hepatocellular carcinoma cells by regulating HMGA2.

The purpose of our study was to investigate the roles of miR-760 and its potential mechanisms in HCC. The functions of miR-760 were identified and measured by MTT, colony formation, transwell, and flow cytometry assays. Luciferase assay was applied to verify the direct binding of miR-760 on HMGA2 3′untranslated region (3′UTR). Then, in vitro experiment was used to investigate the biological effects of miR-760 and HMGA2. Luciferase and ChIP assays were used to detect the validity of SP1 binding sites on the miR-760 promoter. We demonstrated that miR-760 overexpression suppressed cell proliferation, migration, and invasion in HCC. Besides, HMGA2 was demonstrated as a direct target gene of miR-760. Furthermore, we found that methylation may result in the downregulation of miR-760, and SP1 could inhibit the transcription of miR-760. Our study demonstrated that SP1/miR-760/HMGA2 may serve as a molecular regulatory axis for HCC treatment. [ABSTRACT FROM AUTHOR]