MicroRNA-29a Inhibits the Occurrence of Endometrial Carcinoma by Regulating mTOR Signal Pathway Through STAT3

Abstract Background: As a tumor suppressor, miR-29a is involved in the progression of multiple tumors. Its specific role in human endometrial carcinoma (EC) cells remains unclear. Methods: The cells with the overexpression and knockdown of miR-29a were constructed, their effects on EC cell lines were detected, and the binding sites of miR-29a and STAT3 were analyzed. Cell viability was detected by CCK-8 and colony formation assay. The apoptosis was detected by flow cytometry.Results: miR-29a inhibitors increased the survival rate of EC cells, thus inhibiting the apoptosis. miR-29a inhibitors can also promote AKT/mTOR signal pathway. miR-29a mimics lead to diametrically opposite results. The data set analyses showed that STAT3 may be the downstream target of miR-29a. miR-29a inhibited the expression of STAT3 in EC cells. STAT3 promoted cell viability and inhibited apoptosis by activating AKT/mTOR signal pathway. miR-29a mimics can block the proliferation of EC cells induced by STAT3 overexpression and the activation of AKT/mTOR signal pathway. Conclusions: miR-29a inhibits cell growth by targeting STAT3 and inhibiting AKT/mTOR signaling pathway. miR-29a/STAT3/AKT/mTOR may become a new target axis of clinical treatment.