miR‑143‑3p 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 miR‑143‑3p in EM. To explore the role of miR‑143‑3p in EM, functional miRNAs were analyzed via bioinformatics analysis. miR‑143‑3p expression levels in endometriotic stromal cells (ESCs) and normal endometrial stromal cells (NESCs) were measured via reverse transcription‑quantitative PCR. The role of miR‑143‑3p in regulating ESC proliferation and invasion was assessed by performing Cell Counting Kit‑8 and Transwell assays, respectively. miR‑143‑3p expression was significantly upregulated in ESCs compared with NESCs. Functionally, miR‑143‑3p overexpression inhibited ESC proliferation and invasion, whereas miR‑143‑3p knockdown promoted ESC proliferation and invasion. Moreover, miR‑143‑3p 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 miR‑143‑4p mimic group compared with the control group. Moreover, compared with the control group, miR‑143‑3p overexpression significantly decreased the expression levels of autophagy‑related 2B (ATG2B), a newly identified target gene of miR‑143‑3p, in ESCs. ATG2B overexpression reversed miR‑143‑3p overexpression‑mediated inhibition of ESC proliferation and invasion. Collectively, the results of the present study suggested that miR‑143‑3p inhibited EM progression, thus providing a novel target for the development of therapeutic agents against EM.