4.3 Article

Inhibition of lncRNA HOTTIP ameliorated myofibroblast activities and inflammatory cytokines in oral submucous fibrosis

Journal

JOURNAL OF THE FORMOSAN MEDICAL ASSOCIATION
Volume 120, Issue 5, Pages 1188-1193

Publisher

ELSEVIER TAIWAN
DOI: 10.1016/j.jfma.2020.11.013

Keywords

HOTTIP; Myofibroblast; Oral submucous fibrosis

Funding

  1. Chung Shan Medical University Hospital [CSH2018C020]
  2. China Medical University [CMU109N10]
  3. Chung Shan Medical University and Antai Medical Care Cooperation Antai TianSheng Memorial Hospital [CSMUTSMH10901]
  4. Ministry of Science and Technology in Taiwan [MOST 108-2314-B-040-016]

Ask authors/readers for more resources

The study found that HOTTIP is overexpressed in oral submucous fibrosis (OSF) tissues and positively correlated with several fibrosis markers. Inhibiting HOTTIP can reduce the expression of myofibroblast markers and activities, as well as decrease the production of pro-inflammatory cytokines.
Background/Purpose: Long non-coding RNA HOXA transcript at the distal tip (HOTTIP) has been reported to contribute to multiple carcinomas, but whether it involves in the progression of precancerous conditions remains to be determined. Oral submucous fibrosis (OSF) has been known as an oral potentially malignant disorder and attributed to the persistent activation of the myofibroblast. Methods: The relative expression of HOTTIP in OSF tissues has been employed by RNA sequencing and RT-PCR analysis. HOTTIP associated myofibroblasts activities and markers in fibrotic buccal mucosal fibroblast (fBMFs) through loss of function approaches have been evaluated. Results: In the present study, we found that the expression of HOTTIP was overexpressed in the OSF tissues and positively correlated with several fibrosis markers. To investigate its significance of myofibroblast activation, we first verified the expression level of HOTTIP in the patient-derived fibrotic buccal mucosal fibroblast (fBMFs) was upregulated and conducted the shRNA-mediated knockdown experiment to inhibit its expression followed by numerous examinations. We demonstrated that suppression of HOTTIP downregulated the expression of myofibroblast marker, alpha-SMA, and type I collagen along with the diminished myofibroblast activities (collagen gel contraction and migration capacities). Furthermore, we showed that silencing HOTTIP lessened the production of various pro-inflammatory cytokines (IL-6 and TNF-alpha). Conclusion: Collectively, our results suggest that HOTTIP plays a crucial role in the persistent activation of myofibroblasts as well as the chronic inflammation and collagen deposition. Copyright (C) 2021, Formosan Medical Association. Published by Elsevier Taiwan LLC.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.3
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available