Fig. 7
From: Targeting PSAT1 to mitigate metastasis in tumors with p53-72Pro variant
A schematic model illustrating the molecular mechanism of metabolic reprogramming and therapeutic strategies in patients harboring p5372P. PSAT1 interacts with p53-72P. Glucose deprivation enhances this interaction and leads to the dissociation of PGC-1α from p53-72P and subsequent nuclear translocation of PGC-1α, which promotes mitochondrial function and tumor metastasis. Interfering with PSAT1 by serine supplementation or AOA treatment can inhibit the interaction of PSAT1 and p53-72P, leading to decreased nuclear translocation of PGC-1α and impaired mitochondrial function and tumor metastasis
