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Published on: July 20, 2019

NSAID activated gene (NAG-1), a modulator of tumorigenesis

Thomas E Eling1, Seung Joon Baek, Minsub Shim

  • 1National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA. eling@niehs.nih.gov

Journal of Biochemistry and Molecular Biology
|November 30, 2006
PubMed

Insights

NSAID activated gene (NAG-1) shows dual roles in cancer, potentially suppressing tumors early on but promoting them later. Its expression is linked to cell survival and modulated by tumor suppressor pathways.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • NSAID activated gene (NAG-1) is a TGF-beta superfamily member implicated in tumor development.
  • NAG-1 exhibits contradictory roles, with evidence suggesting both anti-tumorigenic and pro-tumorigenic activities.

Purpose of the Study:

  • To investigate the complex role of NAG-1 in tumor progression and development.
  • To explore the regulatory pathways influencing NAG-1 expression.

Main Methods:

  • Analysis of NAG-1 expression in cancer cells and transgenic mice models.
  • Investigating the effects of drug treatments and pathway inhibitions (e.g., cyclooxygenase inhibitors, AKT/GSK-3beta pathway) on NAG-1 levels.

Main Results:

  • Overexpression of NAG-1 induced growth arrest and apoptosis, indicating anti-tumorigenic effects.
  • Transgenic mice expressing NAG-1 resisted intestinal tumor formation.
  • High NAG-1 expression was observed in established tumors, suggesting a pro-tumorigenic role in later stages.
  • NAG-1 expression is upregulated by tumor-preventive agents and pathway modulators like p53, EGR-1, and AKT/GSK-3beta inhibitors.

Conclusions:

  • NAG-1's function appears context-dependent, acting as a tumor suppressor in early stages and potentially promoting tumor progression later.
  • NAG-1 expression is intricately regulated by tumor suppressor pathways and influences cell survival, modulating overall tumor progression.

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