Always Awake (IMAGE)
Caption
Oncogenic MYC disrupts the molecular clock and alters circadian glucose metabolism and glutaminolysis in favor of growth-related biosynthesis in cancer cells. Both MYC and N-MYC upregulate REV-ERBa, which suppresses BMAL1 expression and oscillations. High REV-ERBa or low BMAL1 predicts poor clinical outcome in N-MYC-driven human neuroblastomas.
Credit
Perelman School of Medicine, University of Pennsylvania; <em>Cell Metabolism</em>
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