LINC00312/YBX1 Axis Regulates Myofibroblast Activities in Oral Submucous Fibrosis

International Journal of Molecular Sciences

Pei-Ming Chu¹  Pei-Ling Hsieh¹  Cheng-Chia Yu²  Yi-Wen Liao²  Chuan-Hang Yu²  Lo-Lin Tsai³  Chih-Yuan Fang³ 

[1] Department of Anatomy, School of Medicine, China Medical University, Taichung 404, Taiwan;School of Dentistry, Chung Shan Medical University, Taichung 40201, Taiwan;School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei 110, Taiwan;

关键词: LINC00312;    YBX1;    oral submucous fibrosis;    myofibroblast;   

DOI  :  10.3390/ijms21082979

来源: DOAJ

【 摘 要 】

Oral submucous fibrosis (OSF) has been recognized as a precancerous disorder in the oral cavity. Great effort has been made to inhibit the malignant progression of OSF over the past decades, but the cure of this fibrosis disease has not been discovered. In the present study, we found that a long noncoding RNA, LINC00312, was upregulated in OSF tissues, and positively associated with several fibrosis factors, such as α-SMA, type I collagen, and fibronectin. As such, we sought to investigate the role of LINC00312 in OSF progression and identify its interacting factor that mediated oral fibrogenesis. Our results showed that the inhibition of LINC00312 downregulated the myofibroblast activities, including collagen gel contractility, transwell migration, and wound healing, as well as the gene expression of myofibroblast markers. We verified that YBX1 was a downstream factor of LINC00312 and revealed that the downregulation of YBX1 repressed the gene expression of α-SMA and p-Smad2 along with the reduced myofibroblast phenotypes. Most importantly, we demonstrated that the LINC00312-induced myofibroblast activities were reverted by the knockdown of YBX1, suggesting that the LINC00312-mediated myofibroblast transdifferentiation was through YBX1. Collectively, our findings revealed that the LINC00312/ YBX1 axis may serve as a target for the development of therapies against OSF.

【 授权许可】

Unknown