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Cysteine dioxygenase 1 is a metabolic liability for non-small cell lung cancer

Yun Pyo Kang1, Laura Torrente1, Aimee Falzone1

  • 1Department of Cancer Physiology, H Lee Moffitt Cancer Center and Research Institute, Tampa, United States.

Elife
|May 21, 2019
PubMed

Insights

Nuclear factor erythroid 2-related factor 2 (NRF2) impacts cell metabolism by increasing cysteine. Its regulation of cysteine dioxygenase 1 (CDO1) is crucial, as CDO1 silencing aids non-small cell lung cancer (NSCLC) proliferation.

Area of Science:

  • Cellular metabolism
  • Cancer biology
  • Molecular regulation

Background:

  • Nuclear factor erythroid 2-related factor 2 (NRF2) is a key regulator of cellular metabolism.
  • Studies in cancer cells are complicated by mutations and tumor-specific pressures.
  • Understanding NRF2's direct metabolic effects requires non-transformed cell models.

Purpose of the Study:

  • To investigate the immediate effects of NRF2 on cellular metabolism using genetically engineered primary murine cells.
  • To elucidate the role of cysteine metabolism and its regulators in NRF2-mediated cellular processes.
  • To determine the significance of CDO1 in NRF2-regulated metabolism and its relevance to non-small cell lung cancer (NSCLC).

Main Methods:

  • Utilized genetically engineered, non-transformed primary murine cells to isolate NRF2 effects.
  • Analyzed the impact of NRF2 on intracellular cysteine levels.
  • Investigated the function of cysteine dioxygenase 1 (CDO1) in cysteine metabolism.
  • Examined CDO1 promoter methylation in human NSCLC with KEAP1 mutations.

Main Results:

  • NRF2 promotes intracellular cysteine accumulation.
  • NRF2 engages the cysteine homeostatic control mechanism involving CDO1.
  • CDO1 catalyzes cysteine to cysteine sulfinic acid (CSA).
  • CDO1 is silenced by promoter methylation in KEAP1-mutant NSCLC.
  • CDO1 silencing enhances NSCLC proliferation by limiting futile cysteine metabolism and NADPH depletion.

Conclusions:

  • CDO1 functions as a metabolic regulator, controlling cysteine levels and preventing the formation of toxic byproducts.
  • CDO1 silencing represents a metabolic liability for NSCLC cells, particularly those with NRF2/KEAP1 mutations.
  • Targeting CDO1 or related pathways could offer therapeutic strategies for NSCLC.
Keywords:
CDO1KEAP1NRF2biochemistrycancer biologychemical biologycysteinehumanmousemouse modelsulfite

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