miR­143­3p inhibits endometriotic stromal cell proliferation and invasion by inactivating autophagy in endometriosis.

Endometriosis (EM) is a multifactorial and debilitating chronic benign gynecological disease, but the pathogenesis of the disease is not completely understood. Dysregulated expression of microRNAs (miRNA/miR) is associated with the etiology of EM due to their role in regulating endometrial stromal cell proliferation and invasion. The present study aimed to identify the functions and mechanisms underlying miR­143­3p in EM. To explore the role of miR­143­3p in EM, functional miRNAs were analyzed via bioinformatics analysis. miR­143­3p expression levels in endometriotic stromal cells (ESCs) and normal endometrial stromal cells (NESCs) were measured via reverse transcription­quantitative PCR. The role of miR­143­3p in regulating ESC proliferation and invasion was assessed by performing Cell Counting Kit­8 and Transwell assays, respectively. miR­143­3p expression was significantly upregulated in ESCs compared with NESCs. Functionally, miR­143­3p overexpression inhibited ESC proliferation and invasion, whereas miR­143­3p knockdown promoted ESC proliferation and invasion. Moreover, miR­143­3p inhibited autophagy activation in ESCs, as indicated by decreased green puncta, which represented autophagic vacuoles, decreased microtubule associated protein 1 light chain 3α expression and increased p62 expression in the miR­143­4p mimic group compared with the control group. Moreover, compared with the control group, miR­143­3p overexpression significantly decreased the expression levels of autophagy­related 2B (ATG2B), a newly identified target gene of miR­143­3p, in ESCs. ATG2B overexpression reversed miR­143­3p overexpression­mediated inhibition of ESC proliferation and invasion. Collectively, the results of the present study suggested that miR­143­3p inhibited EM progression, thus providing a novel target for the development of therapeutic agents against EM.