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Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
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FTO demethylates YAP mRNA promoting oral squamous cell carcinoma tumorigenesis

Dian-Qi Li1, Ci-Cheng Huang1, Guang Zhang1

  • 1Department of Oral and Maxillofacial Surgery, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Neoplasma
|November 15, 2021
PubMed

Insights

The fat mass and obesity-associated (FTO) gene, an m6A demethylase, promotes oral squamous cell carcinoma (OSCC) by stabilizing the oncogene YAP1. Targeting FTO offers a potential therapeutic strategy for OSCC patients.

Area of Science:

  • Epigenetics
  • Cancer Biology
  • Molecular Oncology

Background:

  • N6-methyladenosine (m6A) is a prevalent reversible mRNA modification.
  • Fat mass and obesity-associated (FTO) protein acts as an m6A demethylase.
  • FTO's role in oral squamous cell carcinoma (OSCC) remains largely unexplored.

Purpose of the Study:

  • To investigate the function of FTO in OSCC.
  • To elucidate the molecular mechanisms underlying FTO's role in OSCC progression.
  • To evaluate FTO as a potential therapeutic target for OSCC.

Main Methods:

  • Analysis of FTO mRNA and protein expression in OSCC cell lines and tissues.
  • Correlation of FTO levels with clinical parameters and patient survival.
  • Functional studies involving FTO knockdown in OSCC cells.
  • Investigation of FTO's impact on YAP1 mRNA modification and degradation.

Main Results:

  • Elevated FTO expression in OSCC tissues and cell lines.
  • High FTO levels associated with advanced tumor stage, poor differentiation, and reduced survival.
  • FTO knockdown suppressed OSCC cell proliferation, colony formation, and tumor growth.
  • FTO depletion enhanced YAP1 mRNA m6A modification, leading to decreased YAP1 mRNA stability and degradation.
  • FTO's nucleocytoplasmic shuttling is crucial for YAP1 mRNA decay mediated by YTHDF2.

Conclusions:

  • FTO promotes OSCC progression by regulating YAP1 mRNA stability.
  • The FTO/YAP1 axis represents a promising therapeutic target for OSCC intervention.

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