miR-205-5p contributes to paclitaxel resistance and progression of endometrial cancer by downregulating FOXO1.

Endometrial cancer (EC) is one of the most frequent malignancies occurring in female genital system. miR-205-5p has been reported to involve in the progression of multiple malignancies, including EC. However, the detail function and mechanism of miR-205-5p in chemoresistance of EC have not been defined. qRT-PCR assay was performed to detect miR-205-5p abundance in EC tissues and cell lines. The sensitivity of HEC-1-A and RL95-2 cells to PTX was assessed based on the results of IC50. MTT and flow cytometry (FCM) analyses were carried out to determine cell proliferation and apoptosis. Bioinformatics, luciferase, RNA immunoprecipitation (RIP) and western blot analyses were employed to confirm the true interaction between miR-205-5p and FOXO1. Functional restoration experiments were carried out to explore the regulatory mechanism of miR-205-5p in PTX sensitivity and cell growth. miR-205-5p was upregulated in EC tissues and cell lines compared with respective control. Knockdown of miR-205-5p enhanced PTX-sensitivity of EC cells and induced cell growth, which was reflected by the decreased cell proliferation and increased apoptosis. FOXO1 was identified to be a target of miR-205-5p. Elevated miR-205-5p expression reversed FOXO1-enhanced chemosensitivity and cell growth. miR-205-5p enhanced PTX-resistance and contributed to tumorigenesis of EC cells through directly targeting FOXO1. These data shed light on a novel regulation of miR-205-5p in EC, providing a potential therapeutic target for EC patients with PTX resistance.