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- Che-Yi Lin, Yi-Wen Liao, Pei-Ling Hsieh, Ming-Yi Lu, Chih-Yu Peng, Pei-Ming Chu, Hui-Wen Yang, Yu-Feng Huang, Cheng-Chia Yu, and Chuan-Hang Yu.
- Department of Oral and Maxillofacial Surgery, Chi Mei Hospital, Liouying, Tainan, Taiwan.
- J Formos Med Assoc. 2018 Aug 1; 117 (8): 727-733.
Background/PurposeEmerging 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.MethodsQuantitative 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 α-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.ResultsThe 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.ConclusionWe 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 α-SMA, indicating its potential contribution in OSF pathogenesis.Copyright © 2017. Published by Elsevier B.V.
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