Paris-based Institut Necker-Enfants Malades’ Cecilia Patitucci, PhD, and colleagues combined preclinical mouse models of liver cancer with genetic studies of human liver biopsies to identify putative therapeutic targets in relation to liver steatosis and cancer.
Here’s what they found.
1. “Protumoral interaction of Akt2 signaling with hepatocyte nuclear factor 1a and PPARy transcription factors are master regulators of hepatocyte and adipocyte differentiation, respectively,” according to the study.
2. Akt2 phosphorylates and inhibits HNF1a. That stops hepatic PPARy suppression and promotes tumorigenesis.
3. Pharmacological PPARy inhibition is effective in a preclinical murine model of steatosis-associated liver cancer.
Researchers concluded, “Taken together, our studies in humans and mice reveal that Akt2 controls hepatic tumorigenesis through crosstalk between HNF1a and PPARy.
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