Targeting Thyroid Receptor Interacting Protein 6 by MicroRNA-589-5p Inhibits Cell Proliferation, Migration, and Invasion in Endometrial Carcinoma

Background: MicroRNA-589-5p (miR-589-5p) has been recently reported to be aberrantly regulated in hepatocellular carcinoma, but its functional role and molecular mechanisms still remains unknown in the endometrial carcinoma (EC) as one of the most common female malignancies. Methods: EC tissues and adjacent tissues were collected to determine the expression of miR-589-5p and thyroid receptor interacting protein 6 (TRIP6) using quantitative real time-PCR. Subsequently, two EC cell lines HEC-1B and AN3CA were transfected with miR-589-5p to achieve miR-589-5p overexpression. Using Cell Counting Kit-8 (CCK-8), a wound healing assay and the Transwell assay, we analyzed cell proliferation, migration and invasion. Dual-luciferase reporter assay confirmed that thyroid receptor interacting protein 6 (TRIP6) was a direct target of miR-589-5p. Results: We first observed that miR-589-5p was down-regulated in EC tissues compared with normal endometrial tissues. MiR-589-5p overexpression significantly suppressed EC cell proliferation, migration and invasion. Thyroid receptor interacting protein 6 (TRIP6) was a direct target of miR-589-5p. Besides, TRIP6 knockdown presented similar effects on cell proliferation, migration and invasion to miR-589-5p overexpression. Furthermore, TRIP6 knockdown efficiently enhanced the effects of miR-589-5p on the above cellular function. Moreover, miR-589-5p up-regulated E-cadherin expression, but down-regulated N-cadherin and Vimentin by targeting TRIP6. Conclusions: In summary, miR-589-5p might function as a tumor suppressor by targeting TRIP6, which will provide new insights into the molecular mechanism underlying the development of EC.