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Oncogenic potential of Nrf2 and its principal target protein heme oxygenase-1

Hye-Kyung Na1, Young-Joon Surh2

  • 1Department of Food & Nutrition, College of Human Ecology, Sungshin Women's University, Seoul 142-732, South Korea.

Free Radical Biology & Medicine
|November 9, 2013
PubMed

Insights

Nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) are crucial for cellular defense but are paradoxically hijacked by cancer. Elevated Nrf2 and HO-1 promote tumor growth, metastasis, and treatment resistance.

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Oncology

Background:

  • Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key regulator of cellular defense against oxidative stress and various insults.
  • Nrf2 orchestrates the expression of cytoprotective proteins, notably heme oxygenase-1 (HO-1).
  • Recent evidence reveals oncogenic roles for both Nrf2 and HO-1 in cancer progression.

Purpose of the Study:

  • To review the dual role of the Nrf2-HO-1 axis in cancer.
  • To highlight how cancer cells exploit this pathway for growth and survival.
  • To discuss Nrf2 and HO-1 as potential therapeutic targets in oncology.

Main Methods:

  • Literature review of recent studies on Nrf2 and HO-1 in cancer.
  • Analysis of the role of Nrf2-HO-1 in tumor microenvironment modulation.
  • Examination of Nrf2-HO-1 involvement in cancer cell proliferation, metastasis, and treatment resistance.

Main Results:

  • Elevated Nrf2 and HO-1 levels are observed in numerous human malignancies.
  • The Nrf2-HO-1 pathway promotes cancer cell proliferation, angiogenesis, and metastasis.
  • This axis confers resistance to chemotherapy, radiotherapy, and photodynamic therapy.

Conclusions:

  • The cellular stress response mediated by Nrf2-HO-1 is co-opted by cancer cells for survival and proliferation.
  • Targeting the Nrf2-HO-1 pathway presents a promising therapeutic strategy for cancer management.
  • Further research into inhibiting Nrf2 and HO-1 could lead to novel cancer treatments.
Keywords:
Adaptive survival responseAntioxidant response elementsChemoresistanceFree radicalsHeme oxygenase-1Nrf2RadioresistanceRedox balance

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