This report highlights the role of SESN2 in the regulation of glutamine-dependent activation of the mitochondrial biogenesis marker peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) under glucose scarcity in liver cancer cells (HepG2).
Finally, we observed that pharmacological inhibition of PPARγ is therapeutically effective in a preclinical murine model of steatosis-associated liver cancer.
Taken together, these results provide new evidence for the action mechanisms of PPARγ in carcinogenesis of HCC, and upon further investigation, PPARγ could be developed as a new target for the treatment of liver cancer.
In order to determine whether PPARγ plays a central role in HCC, we screened for PPARγ expression in liver cancer patient tissues and differentially differentiated HCC cell lines (HA22T, Huh-7, Hep3B and HepG2).
Pharmacologically, they also displayed diminished PPAR(γ) binding and ap2 gene expression in a mouse pre-adipocyte cell line 3T3-L1, but enhanced anti-cancer properties based on the suppression of liver cancer cell line (Huh-7) proliferation and the expression of tumor marker, afp.