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LncRNA AFAP1‐AS1 regulates proliferation and apoptosis of endometriosis through activating STAT3 / TGF ‐β/Smad signaling via miR ‐424‐5p
Author(s) -
Huan Qing,
Cheng ShuChao,
Du ZhanHui,
Ma HuiFen,
Li Cheng
Publication year - 2021
Publication title -
journal of obstetrics and gynaecology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 50
eISSN - 1447-0756
pISSN - 1341-8076
DOI - 10.1111/jog.14801
Subject(s) - gene knockdown , gene silencing , cancer research , stat3 , apoptosis , smad , cell growth , signal transduction , medicine , biology , microbiology and biotechnology , gene , biochemistry , genetics
Aim Endometriosis is a common gynecological disorder characterized by chronic pelvic pain and infertility, which negatively affects women's health worldwide. AFAP1‐AS1 has been implicated in endometriosis lesions recently, but its mechanism of endometriosis progression remains unclear. Methods Endometrial stromal cells (ESCs) were used to identify the role of AFAP1‐AS1 in endometriosis. The migratory capability was determined by transwell. Gene and protein expressions were identified by quantitative real‐time polymerase chain reaction (qRT‐PCR) and Western blotting. Cell viability and apoptosis were detected by MTT assays and flow cytometry, respectively. Luciferase report assays were used to identify the interaction of AFAP1‐AS1, miR‐424‐5p and signal transducer and activator of transcription 3 (STAT3). Results AFAP1‐AS1 knockdown or miR‐424‐5p overexpression inhibited proliferation and migration, and promoted apoptosis in ESCs. In addition, knockdown of AFAP1‐AS1 repressed the expression of ki‐67 and Bcl‐2, and promoted the levels of cleaved caspase‐3 and Bax. Furthermore, knockdown of AFAP1‐AS1 inhibited the conversion of E‐cadherin to N‐cadherin and the expression of Snail. Moreover, AFAP1‐AS1 activated the STAT3/transforming growth factor‐β1 (TGF‐β1)/Smad2 axis via directly targeting miR‐424‐5p. The regulatory effect of AFAP1‐AS1 silencing in ESC migration, proliferation, and apoptosis was reversed by miR‐424‐5p inhibition or STAT3 overexpression. Conclusions AFAP1‐AS1 silencing could inhibit cell proliferation and promote apoptosis by regulating STAT3/TGF‐β/Smad signaling pathway via targeting miR‐424‐5p in ESCs. AFAP1‐AS1 may be a potential therapeutic target of controlling the progression of endometriosis.