Journal
JOURNAL OF THE FORMOSAN MEDICAL ASSOCIATION
Volume 117, Issue 8, Pages 727-733Publisher
ELSEVIER TAIWAN
DOI: 10.1016/j.jfma.2017.09.012
Keywords
IncRNA GAS5-AS1; Myofibroblasts; Oral submucous fibrosis
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Funding
- Chung Shan Medical University Hospital [CSH-2017-C-033]
- Ministry of Science and Technology [MOST 106-2314-B-040-004-MY3]
- Chung Shan Medical University in Taiwan
- Chi Mei Hospital in Taiwan [CSMU-CMMC-105-04, CMCSMU10506]
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Background/Purpose: Emerging research findings suggest that long non-coding RNAs (lncRNAs) are key regulators to fibrosis formation. Nevertheless, the role of lncRNA GAS5-AS1 in the progression of precancerous oral submucous fibrosis (OSF) remains to be elucidated. Methods: Quantitative real-time PCR were used to examine the expression of GAS5-AS1 in OSF tissues. The activities of myofibroblasts, including collagen contractility and cell migration, as well as the marker a-smooth muscle actin (SMA) were assessed following overexpression of GAS5-AS1. Also, we analyzed the expression of Smad activity in order to gain insight into the downstream regulator. Results: The level of GAS5-AS1 was found significantly downregulated in the OSF tissues and fibrotic buccal mucosal fibroblasts (fBMFs). Ectopic expression of GAS5-AS1 significantly reduced the abilities of collagen gel contraction and migration in fBMFs or arecoline-treated BMFs. Moreover, we have shown that overexpression of GAS5-AS1 inhibited the expression of p-Smad and the marker of myofibroblasts. Conclusion: We showed the reduced expression of GAS5-AS1 in OSF tissues and demonstrated its effect on the myofibroblast activities and the level of p-Smad and alpha-SMA, indicating its potential contribution in OSF pathogenesis. Copyright (C) 2017, Formosan Medical Association. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license(http://creativecommons.org/licenses/by-nc-nd/4.0/).
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