LINC00312/YBX1 Axis Regulates Myofibroblast Activities in Oral Submucous Fibrosis

Chuan-Hang Yu1,2,3, Chih-Yuan Fang4,5, Cheng-Chia Yu1,2,3

  • 1School of Dentistry, Chung Shan Medical University, Taichung 40201, Taiwan.

Insights

Researchers identified LINC00312 as a key factor in oral submucous fibrosis (OSF) progression. Targeting the LINC00312/YBX1 pathway shows promise for developing new therapies for this precancerous oral condition.

Area of Science:

  • Oral pathology
  • Molecular biology
  • Oncology

Background:

  • Oral submucous fibrosis (OSF) is a precancerous condition with no known cure.
  • Malignant progression of OSF remains a significant clinical challenge.
  • Understanding the molecular mechanisms driving OSF is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the role of long noncoding RNA LINC00312 in oral submucous fibrosis (OSF) progression.
  • To identify the downstream interacting factor of LINC00312 involved in oral fibrogenesis.
  • To explore the therapeutic potential of targeting the LINC00312/YBX1 axis in OSF.

Main Methods:

  • Analysis of LINC00312 expression in OSF tissues.
  • Inhibition of LINC00312 and assessment of myofibroblast activity (e.g., collagen gel contractility, migration, wound healing).
  • Verification of YBX1 as a downstream target and investigation of its role in myofibroblast gene expression (α-SMA, p-Smad2).

Main Results:

  • LINC00312 was upregulated in OSF tissues and correlated with fibrosis markers.
  • LINC00312 inhibition reduced myofibroblast activity and marker gene expression.
  • YBX1 was identified as a downstream mediator; its downregulation repressed myofibroblast phenotypes.
  • Knockdown of YBX1 reversed LINC00312-induced myofibroblast activities, confirming the LINC00312/YBX1 axis.

Conclusions:

  • The LINC00312/YBX1 axis plays a critical role in mediating myofibroblast transdifferentiation in OSF.
  • This axis represents a potential therapeutic target for treating oral submucous fibrosis.
  • Further research into targeting LINC00312 and YBX1 could lead to novel OSF therapies.

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