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Role of the KEAP1-NRF2 Axis in Renal Cell Carcinoma

Sara Clerici1, Alessandra Boletta1

  • 1IRCCS San Raffaele Scientific Institute, Molecular Basis of Cystic Kidney Diseases, Division of Genetics and Cell Biology, 20132 Milan, Italy.

Cancers
|November 25, 2020
PubMed

Insights

Nuclear factor erythroid 2-related factor 2 (NRF2) normally protects cells from stress. However, its overactivation in kidney cancer promotes tumor growth and treatment resistance by disrupting the KEAP1-NRF2 pathway.

Area of Science:

  • Molecular biology
  • Oncology
  • Cellular stress response

Background:

  • Nuclear factor erythroid 2-related factor 2 (NRF2) is a key transcription factor regulating cellular antioxidant responses and cytoprotection against stress.
  • While essential for normal kidney function, aberrant NRF2 activation is implicated in the progression, metastasis, and therapeutic resistance of renal cell carcinoma (RCC).

Purpose of the Study:

  • To investigate the role of NRF2 hyperactivation in renal cell carcinoma (RCC) progression and chemoresistance.
  • To elucidate the molecular mechanisms underlying NRF2 dysregulation in RCC, focusing on the KEAP1-NRF2 axis.

Main Methods:

  • Review and analysis of molecular mechanisms governing NRF2 activity in cancer.
  • Focus on the convergence of altered tumor pathways leading to KEAP1-NRF2 axis dysregulation in RCC.

Main Results:

  • NRF2 hyperactivation contributes to tumor progression and chemoresistance in RCC.
  • Altered signaling pathways in RCC converge to dysregulate the KEAP1-NRF2 axis.

Conclusions:

  • Understanding NRF2 hyperactivation mechanisms in RCC is critical for developing new therapeutic strategies.
  • Targeting the KEAP1-NRF2 axis presents a potential therapeutic avenue for renal cell carcinoma.
Keywords:
KEAP1NRF2PRCCccRCCkidney injury

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