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Related Concept Videos

  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Pklr Promotes Colorectal Cancer Liver Colonization Through Induction Of Glutathione Synthesis.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Pklr Promotes Colorectal Cancer Liver Colonization Through Induction Of Glutathione Synthesis.

Related Experiment Video

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
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PKLR promotes colorectal cancer liver colonization through induction of glutathione synthesis.

Alexander Nguyen, Jia Min Loo, Rohit Mital

    The Journal of Clinical Investigation
    |January 20, 2016

    View abstract on PubMed

    Summary
    This summary is machine-generated.

    Liver and red blood cell pyruvate kinase (PKLR) drives colorectal cancer liver metastasis by boosting glutathione, an antioxidant crucial for cancer cell survival in oxygen-deprived tumor cores. Targeting this metabolic pathway shows clinical potential.

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    Portal Vein Injection of Colorectal Cancer Organoids to Study the Liver Metastasis Stroma
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    Area of Science:

    • Oncology
    • Metabolism
    • Cancer Metastasis

    Background:

    • Colorectal cancer liver metastasis is a leading cause of cancer mortality.
    • The molecular mechanisms driving liver colonization by colorectal cancer remain incompletely understood.

    Purpose of the Study:

    • To identify genes and pathways critical for colorectal cancer liver metastasis.
    • To investigate the role of pyruvate kinase liver and red blood cell (PKLR) in metastatic colonization.

    Main Methods:

    • Conducted a large-scale in vivo RNA interference (RNAi) screen.
    • Utilized a murine liver colonization model.
    • Analyzed gene expression in patient tumor samples.

    Main Results:

    • PKLR was identified as a driver of liver metastasis and its expression was elevated in patient liver metastases and primary tumors.
  • PKLR enhances cancer cell survival in hypoxic, dense tumor cores by increasing glutathione levels.
  • Inhibition of glutathione synthesis impaired cancer cell survival and reduced metastasis in preclinical models.

    • Conclusions:

    • PKLR-mediated metabolic reprogramming, specifically glutathione synthesis, is crucial for colorectal cancer liver metastasis.
    • Targeting the glutathione synthesis pathway represents a potential therapeutic strategy for colorectal cancer patients with metastatic disease.