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Expression and correlation of the long noncoding RNA PDIA3P and FAK/TGF-β pathway in oral submucous fibrosis rats

  • 0Department of Stomatology, Affiliated Hospital of Jinggangshan University, Ji'an Clinical Research Center for Oral Diseases, Ji'an, Jiangxi 343000, China.
Journal of Stomatology, Oral and Maxillofacial Surgery +

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January 5, 2025

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January 5, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Upregulating long noncoding RNA PDIA3P (lncRNA PDIA3P) and the FAK/TGF-β pathway accelerates oral submucous fibrosis (OSF) development. Conversely, reducing their activity may prevent OSF, offering potential therapeutic targets for this life-threatening oral condition.

Area Of Science

  • Oral pathology
  • Molecular biology
  • Cancer research

Background

  • Oral submucous fibrosis (OSF) is a severe oral condition with a high risk of progressing to oral squamous cell carcinoma.
  • Current treatments for OSF are limited, and its underlying molecular mechanisms remain unclear.
  • Understanding OSF pathogenesis is crucial for developing effective preventative and therapeutic strategies.

Purpose Of The Study

  • To elucidate the molecular mechanisms of long noncoding RNA PDIA3P (lncRNA PDIA3P) and the FAK/TGF-β pathway in the development of OSF.
  • To investigate the role of lncRNA PDIA3P and FAK/TGF-β signaling in an established OSF mouse model.
  • To identify potential molecular targets for preventing or treating OSF.

Main Methods

  • Establishment of an OSF mouse model using arecoline solution.
  • Collection and analysis of blood and oral submucosal tissue samples.
  • Utilized HE staining, immunofluorescence, Western blot, and qRT-PCR to analyze molecular changes.

Main Results

  • Upregulation of the FAK/TGF-β signaling pathway was found to accelerate the OSF process.
  • Downregulation of the FAK/TGF-β signaling pathway demonstrated a preventative effect on OSF.
  • Enhanced activity of lncRNA PDIA3P was implicated in OSF progression, while its reduction showed preventative potential.

Conclusions

  • The study concludes that upregulating lncRNA PDIA3P and the FAK/TGF-β pathway can accelerate the process of OSF.
  • These findings suggest that targeting lncRNA PDIA3P and the FAK/TGF-β pathway could be a viable strategy for preventing OSF development.

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