Abstract
LDH-A Acetylation: Implication in Cancer
Highlights
Upregulation of lactate dehydrogenase A (LDH-A) is commonly observed in many tumor types
Instead of entering mitochondria to fuel the tricarbolic acid (TCA) cycle and oxidative phosphorylation for efficient energy production, a large fraction of pyruvate in cancer cells is converted into lactate by LDH, accompanied by NAD+ regeneration to maintain high glycolysis rate (Figure1)
In many tumors, elevated LDH-A levels have been correlated with poor prognosis and resistance to chemotherapy and radiotherapy
Summary
Upregulation of lactate dehydrogenase A (LDH-A) is commonly observed in many tumor types. Instead of entering mitochondria to fuel the tricarbolic acid (TCA) cycle and oxidative phosphorylation for efficient energy production, a large fraction of pyruvate in cancer cells is converted into lactate by LDH, accompanied by NAD+ regeneration to maintain high glycolysis rate (Figure1). In many tumors, elevated LDH-A levels have been correlated with poor prognosis and resistance to chemotherapy and radiotherapy. It has been reported that inhibition of LDH-A by either RNA interference or pharmacological agents blocks tumor progression in vivo, supporting an important role of elevated LDH-A in tumorigenesis and LDH-A as a potential therapeutic target.
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