MiR-20a-5p inhibits endometrial cancer progression by targeting janus kinase 1.

ABSTRACT: Endometrial cancer (EC) is a multi-factorial disease of which pathogenesis has not been fully elucidated. The function and underlying mechanism of microRNA-20a-5p (miR-20a-5p) in EC remain poorly understood. The present study aimed to analyze the association between miR-20a-5p expression and the clinicopathological characteristics of patients with EC. Whether miR-20a-5p could inhibit EC progression by targeting janus kinase 1 (Jak1) was subsequently investigated. To do so, human EC tissues and paracancerous tissues were collected from 47 patients with EC. miR-20a-5p and Jak1 mRNA and protein expression was determined by reverse transcription quantitative PCR and western blotting, respectively. Cell proliferation, invasive ability and adhesion were investigated by MTT, Matrigel invasion and cell adhesion assays, respectively. Dual luciferase reporter assay was used to verify whether miR-20a-5p could directly target Jak1. The results demonstrated that miR-20a-5p was downregulated and that Jak1 was upregulated in EC tissues compared with paracancerous tissues. In addition, miR-20a-5p expression and Jak1 expression level were negatively correlated in EC tissues. miR-20a-5p expression was also significantly associated with the depth of myometrial invasion, FIGO stage, histologic grade and lymph node metastasis in patients with EC. Furthermore, Jak1 was identified as a new direct target of miR-20a-5p, and Jak1 overexpression was demonstrated to reverse the effects of miR-20a-5p-mimic on EC cell proliferation, invasive ability and adhesion. Taken together, the results from this study revealed for the first time that miR-20a-5p expression was significantly associated with the clinicopathological characteristics of patients with EC. These findings suggested that miR-20a-5p may act as a tumor suppressor in EC, in part through decreasing Jak1 expression. miR-20a-5p and Jak1 may therefore serve as potential therapeutic targets in EC.

SUBMITTER: He Y 

PROVIDER: S-EPMC8025135 | biostudies-literature |

REPOSITORIES: biostudies-literature