MiR-106a promotes tumor growth, migration, and invasion by targeting <i>BCL2L11</i> in human endometrial adenocarcinoma.

Abstract

Growing evidence indicates that miR-106a is involved in tumor growth and metastasis of cancers, but the participation of miR-106a in endometrial adenocarcinoma (EC) is not clear. BCL2L11 is a member of the BCL-2 family and is located in the outer membrane of mitochondria, where this protein acts as a key regulator of excitotoxic apoptosis, apoptosis-inducing factor translocation, and mitochondrial depolarization. To identify a novel therapeutic target in EC, we studied the roles of miR-106a in the proliferation, apoptosis, and metastasis of EC. The expression levels of miR-106a were measured in tumor tissues of EC by quantitative real-time PCR, and lentiviral transduction was used to verify the function of miR-106a by silencing. Subcutaneous injection of EC cell lines into athymic mice was used to research EC tumor formation. Bioinformatics tools and a luciferase assay were applied to assess the relation between miR-106a and its target. The protein level of the miR-106a target was measured by western blotting. MiR-106a expression was higher in EC tissues compared with their healthy counterparts. Inhibition of expression of miR-106a reduced EC cell migration and invasion <i>in vitro</i> as well as <i>in vivo</i> tumor growth. BCL2L11 mRNA contains a binding site for miR-106a in the 3'untranslated region. <i>BCL2L11</i> was found to be one of miR-106a targets. Altogether, our data suggest that miR-106a inhibits proliferation and invasiveness and induces cell cycle arrest and apoptosis in EC cells by targeting <i>BCL2L11</i>, and therefore miR-106a may serve as a prognostic marker of EC.