LncRNA AFAP1-AS1 regulates proliferation and apoptosis of endometriosis through activating STAT3/TGF-β/Smad signaling via miR-424-5p

Qing Huan, Huan Q, Shu-Chao Cheng, Cheng SC, Shu‐Chao Cheng, Zhan-Hui Du, Zhanhui Du, Du ZH, Huifen Ma, Hui-Fen Ma, Li C, Cheng Li
Journal of Obstetrics and Gynaecology Research · 2021 · vol. 47(7) , pp. 2394–2405 · doi:10.1111/jog.14801 · PMID:33949053 · W3159508852
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LncRNA AFAP1-AS1 promotes endometriosis progression by activating STAT3/TGF-β/Smad signaling via targeting miR-424-5p, thus regulating proliferation and apoptosis.

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Abstract

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.

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Condition tags

endometriosischronic_pelvic_paininfertility

MeSH descriptors

Endometriosis Endometriosis MicroRNAs MicroRNAs RNA, Long Noncoding RNA, Long Noncoding Apoptosis Apoptosis Cell Line, Tumor Cell Line, Tumor Cell Proliferation Cell Proliferation Female Female Humans Humans Signal Transduction Signal Transduction STAT3 Transcription Factor STAT3 Transcription Factor

Citation neighborhood (2-hop)

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (52)

Cited by (19)

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