
A study has shed light on the role of peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1α) in OPMD progression. The study found that knocking down PGC1α inhibited dysplastic oral keratinocyte (DOK) proliferation and tumor growth, leading to S-phase arrest and PI3K/Akt signalling suppression. Mechanistically, reduced PGC1α levels affected mitochondrial function, increasing glycolysis and glucose uptake. Inhibiting PGC1α with SR18292 disrupted oxidative phosphorylation in DOKs. PGC1α emerges as a potential therapeutic target for OPMDs, reprogramming energy metabolism and inhibiting their progression.
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