
Highlights •Prolyl hydroxylase 3 (PHD3) hydroxylates and activates the metabolic enzyme ACC2 •During nutrient abundance, the PHD3/ACC2 axis represses fatty acid oxidation (FAO) •PHD3 is low in AML, fueling a reliance on fats that can be targeted with FAO inhibitors •Re-expressing PHD3 limits FAO via ACC2 and suppresses AML in culture and in vivo
A handful of cancers favor fat over sugar, a propensity that has long mystified scientists. Now, a study from Harvard Medical School reveals how certain tumors develop a taste for fat as their life-sustaining fuel. The findings show how a signaling pathway that normally keeps fat-burning in check goes awry in some cancers, revving up fat consumption and fueling tumor growth.
Specifically, the study found a protein called prolyl hydroxylase ...
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