OBJECTIVETo investigate the regulatory functions and molecular mechanisms of miR211 in hepatocellular carcinoma (HCC).

METHODSReal-time reverse transcription-PCR was used to analyze the expression of miR-211 in 20 paired clinical specimens of HCC and adjacent noncancerous tissues.QGY7703 and HepG2 cells with stimulation or inhibition of miR-211 expression were used to evaluate the effects on malignant phenotypes with the transwell invasion assay. Candidate target genes of miR-211 were identified by bioinformatic screening and verified by the EGFP report assay, real-time PCR and western blotting. Moreover, the regulatory functions of miR-211 on the target genes were investigated by RNA interference and cell phenotype assays.

RESULTSmiR-211 was up-regulated in HCC tissue specimens (t =6.26, P < 0.01).HCC cells overexpressing miR-211 showed greater invasive capacity than cells with inhibited expression (QGY-7703:t =12.59, P < 0.01; HepG2: t =17.82, P < 0.01). Estrogen receptor a (ESR1) was identified and validated as a target gene of miR-211; knockdown of ESR 1 promoted HCC invasive capacity (QGY-7703:t =8.97, P < 0.01; HepG2:t =29.31, P < 0.01).

CONCLUSIONmiR-211 promotes invasion of carcinoma cells by directly targeting ESR1.