NCK1 antisense RNA 1 (NCK1-AS1) exerts pro-fibrosis property in oral mucosa through modulation of miR-137/NCK1 axis

Yu-Feng Huang1,2, Yu-Lei Wei1,3, Shih-Min Wang1,3

  • 1School of Dentistry, Chung Shan Medical University, Taichung, Taiwan.

PubMed
Abstract

Insights

Long non-coding RNA NCK1-AS1 promotes oral submucous fibrosis (OSF) by acting as a sponge for microRNA-137 (miR-137), upregulating NCK1 and myofibroblast activation in this premalignant condition.

Area of Science:

  • Molecular Biology
  • Oncology
  • RNA Biology

Background:

  • Oral submucous fibrosis (OSF) is a premalignant oral condition with unknown pathogenesis.
  • Aberrant expression of non-coding RNAs is observed in OSF, suggesting their role in disease development.

Purpose of the Study:

  • To investigate the functional role of long non-coding RNA NCK1-AS1 in myofibroblast activation in OSF.
  • To elucidate the molecular mechanism by which NCK1-AS1 influences fibrotic buccal mucosal fibroblasts (fBMFs).

Main Methods:

  • Assessed myofibroblast activities using wound healing, collagen gel contraction, and transwell migration assays.
  • Utilized a luciferase-based reporter assay to determine the regulatory mechanism of NCK1-AS1.

Main Results:

  • Silencing NCK1-AS1 reduced myofibroblast activation and fibrosis markers in fBMFs.
  • NCK1-AS1 directly interacted with and suppressed microRNA-137 (miR-137).
  • NCK1 was identified as a target of miR-137, with NCK1-AS1 positively correlating with NCK1 expression.

Conclusions:

  • NCK1-AS1 acts as a molecular sponge for miR-137, inhibiting its suppressive effect on NCK1.
  • This mechanism modulates myofibroblast activation in the context of oral submucous fibrosis.

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