Cited by 28Endometriosis Research and TreatmentCancer-related molecular mechanisms researchTGF-β signaling in diseases

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

Huan, Qing, Cheng, Shu‐Chao, Du, Zhan‐Hui, Ma, Hui‐Fen, Li, Cheng·2021·Journal of obstetrics and gynaecology research

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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Crossref · 10.1111/jog.14801

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  • AFAP1-AS1 silencing can inhibit cell proliferation and promote apoptosis by regulating the STAT3/TGF-β/Smad signaling pathway by targeting miR-424-5p in endometrial stromal cells.

    “AFAP1-AS1 silencing can inhibit cell proliferation and promote apoptosis by regulating the STAT3/TGF-β/Smad signaling pathway by targeting miR-424-5p in endometrial stromal cells [173].”

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Authors
Huan, Q., Cheng, S., Du, Z., Ma, H., & Li, C.
Affiliations
  • Central South University (CN)
  • Shandong University of Traditional Chinese Medicine (CN)
  • Heart Center Qingdao Women and Children's Hospital, Qingdao University Qingdao China
  • National Health Commission Capacity Building and Continuing Education Center Beijing China
  • Reproductive Center, The First People's Hospital of Yueyang Yueyang China
Corresponding author
Huan, Qing
Venue
Journal of obstetrics and gynaecology research
Publisher
Wiley
Published
2021-05-04
Volume
47
Issue
7
Pages
2394-2405
ISSN
  • 1341-8076 (ISSN-L)
  • 1447-0756
OpenAlex
W3159508852
Cited by
28
References
46
Citations by year
2026: 1 · 2025: 6 · 2024: 4 · 2023: 3 · 2022: 10 · 2021: 2
FWCI
4.10
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of obstetrics and gynaecology research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
Keywords
endometriosis, AFAP1-AS1, long non-coding RNA, miR-424-5p, STAT3, TGF-β1/Smad2 signaling, endometrial stromal cells, cell proliferation, apoptosis, cell migration, epithelial-mesenchymal transition, E-cadherin, snails, therapeutic target
MeSH terms
Endometriosis, Female, Humans, Signal Transduction, Transforming Growth Factor beta, Apoptosis, MicroRNAs, Cell Line, Tumor, Cell Proliferation, STAT3 Transcription Factor, RNA, Long Noncoding

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