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Osteopontin is Critical for Hyperactive mTOR-Induced Tumorigenesis in Oral Squamous Cell Carcinoma

Ning Gan1,2,3,4, Sihai Zou1,2,3, Wenming Hang1,2,3

  • 1Stomatological Hospital of Chongqing Medical University, Chongqing 401147, China.

Journal of Cancer
|June 23, 2017
PubMed

Insights

Osteopontin (OPN) is upregulated in oral squamous cell carcinoma (OSCC) and drives tumor growth. Mechanistic target of rapamycin complex 1 (mTORC1) enhances OPN expression, suggesting both are potential therapeutic targets for OSCC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Mechanistic target of rapamycin (mTOR) signaling is implicated in oral squamous cell carcinoma (OSCC) development.
  • The precise molecular mechanisms linking mTOR to OSCC progression are not fully elucidated.

Purpose of the Study:

  • To investigate the role of osteopontin (OPN) in OSCC.
  • To elucidate the relationship between mTOR complex 1 (mTORC1) and OPN expression in OSCC.

Main Methods:

  • Analysis of OPN expression in OSCC tissues and cell lines.
  • Assessment of OPN's effect on OSCC cell proliferation, colony formation, and tumorigenicity.
  • Correlation analysis between mTORC1 activity and OPN levels.
  • Investigation of the regulatory pathway involving mTORC1, ERRα, and OPN.

Main Results:

  • Osteopontin (OPN) expression was significantly increased in OSCC tissues and cell lines.
  • Reduced OPN levels inhibited OSCC cell proliferation, colony formation, and in vivo tumor growth.
  • A positive correlation was observed between mTORC1 activity and OPN expression in OSCC.
  • mTORC1 was found to enhance OPN expression via up-regulation of ERRα.

Conclusions:

  • OPN is a critical downstream target of mTORC1 and plays a crucial role in OSCC development.
  • mTORC1, ERRα, and OPN represent potential therapeutic targets for OSCC treatment, particularly in cases with aberrant mTORC1 signaling.
Keywords:
ERRαOPNOSCC.mTORtumorigenesis

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