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. 2023 Apr;478(4):707-719.
doi: 10.1007/s11010-022-04538-6. Epub 2022 Aug 29.

LncRNA GNAS-AS1 knockdown inhibits keloid cells growth by mediating the miR-188-5p/RUNX2 axis

Yun Liu #  1 , Lei Li #  1 , Jia-Yao Wang  1 , Fei Gao  1 , Xia Lin  1 , Shi-Shuai Lin  2 , Zhi-Yang Qiu  2 , Zun-Hong Liang  3
Affiliations

LncRNA GNAS-AS1 knockdown inhibits keloid cells growth by mediating the miR-188-5p/RUNX2 axis

Yun Liu et al. Mol Cell Biochem. 2023 Apr.

Abstract

Keloid is a common dermis tumor, occurring repeatedly, affecting the quality of patients' life. Long non-coding RNAs (lncRNAs) have crucial regulatory capacities in skin scarring formation and subsequent scar carcinogenesis. The intention of this study was to investigate the mechanism and function of GNAS antisense-1 (GNAS-AS1) in keloids. Clinical samples were collected to evaluate the expression of GNAS-AS1, RUNX2, and miR-188-5p by qRT-PCR. The proliferation, migration, and invasion of HKF cells were detected by CCK-8, wound healing, and Transwell assays. The expression levels of mRNA and protein were examined through qRT-PCR and Western blot assay. Luciferase reporter assay was used to identify the binding relationship among GNAS-AS1, miR-188-5p, and Runt-related transcription factor 2 (RUNX2). GNAS-AS1 and RUNX2 expressions were remarkably enhanced, and miR-188-5p expression was decreased in keloid clinical tissues and HKF cells. GNAS-AS1 overexpression promoted cells proliferation, migration, and invasion, while GNAS-AS1 knockdown had the opposite trend. Furthermore, overexpression of GNAS-AS1 reversed the inhibitory effect of 5-FU on cell proliferation, migration, and invasion. MiR-188-5p inhibition or RUNX2 overexpression could enhance the proliferation, migration, and invasion of HKF cells. GNAS-AS1 targeted miR-188-5p to regulate RUNX2 expression. In addition, the inhibition effects of GNAS-AS1 knockdown on HKF cells could be reversed by inhibition of miR-188-5p or overexpression of RUNX2, while RUNX2 overexpression eliminated the suppressive efficaciousness of miR-188-5p mimics on HKF cells growth. GNAS-AS1 knockdown could regulate the miR-188-5p/RUNX2 signaling axis to inhibit the growth and migration in keloid cells. It is suggested that GNAS-AS1 may become a new target for the prevention and treatment of keloid.

Keywords: GNAS-AS1; Keloid; RUNX2; miR-188-5p.

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References

    1. Huang Y, Wang Y, Lin L, Wang P, Jiang L, Liu J, Wang X (2020) Overexpression of miR-133a-3p inhibits fibrosis and proliferation of keloid fibroblasts by regulating IRF5 to inhibit the TGF-beta/Smad2 pathway. Mol Cell Probes 52:101563. https://doi.org/10.1016/j.mcp.2020.101563 - DOI - PubMed
    1. Cui J, Li Z, Jin C, Jin Z (2020) Knockdown of fibronectin extra domain B suppresses TGF-beta1-mediated cell proliferation and collagen deposition in keloid fibroblasts via AKT/ERK signaling pathway. Biochem Biophys Res Commun 526:1131–1137. https://doi.org/10.1016/j.bbrc.2020.04.021 - DOI - PubMed
    1. Naylor MC, Brissett AE (2012) Current concepts in the etiology and treatment of keloids. Facial Plast Surg 28:504–512. https://doi.org/10.1055/s-0032-1325644 - DOI - PubMed
    1. Andrews JP, Marttala J, Macarak E, Rosenbloom J, Uitto J (2016) Keloids: the paradigm of skin fibrosis—pathomechanisms and treatment. Matrix Biol 51:37–46. https://doi.org/10.1016/j.matbio.2016.01.013 - DOI - PubMed - PMC
    1. Marttala J, Andrews JP, Rosenbloom J, Uitto J (2016) Keloids: animal models and pathologic equivalents to study tissue fibrosis. Matrix Biol 51:47–54. https://doi.org/10.1016/j.matbio.2016.01.014 - DOI - PubMed - PMC

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