MiR-143 inhibits endometrial cancer cell proliferation and metastasis by targeting .

Endometrial cancer (EC) is one of the most commonly diagnosed gynecologic malignancies in the world, with the morbidity rate of over 7%. The mechanism of the pathogenesis has not been specifically elucidated to date, which is imperative for EC treatment. The aim of our study was to investigate the target relationship between miR-143 and mitogen-activated protein kinase 1 () and explore the effect of miR-143 on the endometrial cancers (EC) cells through targeting . We collected EC tissues and adjacent tissues, and transfected miR-143 mimics and siRNA into EC cells with lipofectamine. Reverse transcription-polymerase chain reaction (RT-PCR) and western blot were used to examine the expression of miR-143 and mRNA and the protein expression of . Cell counting kit-8, wound healing assay, flow cytometry and transwell assay were applied to examining the alteration of the proliferation, migration, cell cycle and invasion ability of EC cells. We predicted the targeting gene of miR-143 through bioinformatics analysis. MiR-143 was found under-expressed in EC tissues and cells. Overexpression of miR-143 or knockdown of in human EC cell line HEC-1B inhibited the EC cell proliferation, migration and invasion and induced apoptosis. was verified to be a target gene of miR-143. MiR-143 overexpression could effectively inhibit mRNA and protein expression of in HEC-1B cells. Collectively, miR-143 might inhibit the proliferation, migration and invasion of EC cells, and promote the apoptosis of EC cells by suppressing . These findings provided a view for new and potential therapeutic method for the clinical treatment of EC.