Propofol inhibits proliferation and invasion of endometriotic cells by miR-9-5p/TGFBI axis

Abstract

Endometriosis (EM) is an estrogen-dependent, frequent benign gynecological disease, which reduces the quality of life in EM patients. Propofol regulates the apoptosis of EM. miR-9-5p is decreased in early secretory endometrium, TGFBI is increased in EM, however, their functions in EM remain unclear. This study aimed to investigate the mechanisms underlying the effects of propofol on the proliferation and invasion of EM by regulating miR-9-5p/TGFBI. The proliferation and invasion of ectopic endometrial stromal cells (ESCs) were determined by MTT assay and Transwell assay, respectively. Real-time PCR was applied for the evaluation of miR-9-5p and transforming growth factor-β (TGF-β)-induced gene (TGFBI) mRNA level in ESCs. Western blot was used to examine the protein level of TGFBI protein (TGFBIp) in ESCs. The relation between miR-9-5p and TGFBI was predicted by TargetScan 7.1 and verified by dual luciferase reporter assay. Propofol reduced cell proliferation and invasion, while induced miR-9-5p level and reduced TGFBI/TGFBIp level in ectopic ESCs. Additionally, in ectopic ESCs from patients with EM, miR-9-5p was lower, while TGFBI and TGF-BIp were higher than those from eutopic endometrium and normal endometrium from patients with hysteromyoma. Moreover, propofol reduced proliferation and invasion in ectopic ESCs, which was realized by the regulation of miR-9-5p/TGFBI.