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  4. Down-regulation of miR-29c promotes the progression of oral submucous fibrosis through targeting tropomyosin-1
 
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Down-regulation of miR-29c promotes the progression of oral submucous fibrosis through targeting tropomyosin-1

Journal
Journal of the Formosan Medical Association
Date Issued
2022-06-01
Author(s)
PO-YU YANG  
YI-WEN LIAO  
CHENG-CHIA YU  
DOI
10.1016/j.jfma.2021.10.006
URI
https://www.scopus.com/pages/publications/85117716041
https://scholars.csmu.edu.tw/handle/123456789/24673
Abstract
Background/Purpose: Various microRNAs (miRs) have been found to be associated with the development of the precancerous condition of the oral cavity, oral submucous fibrosis (OSF). The expression of miR-29c is dysregulated in oral cancer, but its role in OSF has not been investigated. The purpose of the study is to investigate the functional role of miR-29c and its target in OSF. Methods: The expression levels of miR-29c in OSF tissues and fibrotic buccal mucosal fibroblasts (fBMFs) were assessed using next-generation sequencing and real-time Polymerase Chain Reaction (PCR) analysis. MiR-29c mimic and inhibitors were employed to examine its functional role of myofibroblast transdifferentiation. In addition, several myofibroblast phenotypes, such as collagen gel contraction and migration were tested, and a luciferase reporter assay was conducted to confirm the relationship between miR-29c and its predicted target, tropomyosin-1 (TPM1). Results: We observed that miR-29c expression was downregulated in fBMFs. fBMFs transfected with miR-29c mimics exhibited reduced migration ability and collagen gel contractility, whereas inhibition of miR-29c in normal BMFs induced the myofibroblast phenotypes. Results from the luciferase reporter assay showed that TPM1 was a direct target of miR-29c and the expression of TPM1 was suppressed in the fBMFs transfected with miR-29c mimics. Besides, we confirmed that the expression of miR-29c was indeed downregulated in OSF specimens. Conclusion: MiR-29c seems to exert an inhibitory effect on myofibroblast activation, such as collagen gel contractility and migration ability, via suppressing TPM1. These results suggested that approaches to upregulate miR-29c may be able to ameliorate the progression of OSF.
Type
journal article
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