PDGFRI3 modulates aerobic glycolysis in osteosarcoma HOS cells via the PI3K/AKT/mTOR/c-Myc pathway

Osteosarcoma is a malignant tumor abundant in vascular tissue, and its rich blood supply may have a significant impact on its metabolic characteristics. PDGFRI3 is a membrane receptor highly expressed in osteosarcoma cells and vascular wall cells, and its effect on osteosarcoma metabolism needs to be further studied. In this study, we discussed the effect and mechanism of action of PDGFRI3 on glucose metabolism in human osteosarcoma (HOS) cells. GSEA, Pearson's correlation test, and PPI correlation analysis indicated positive regulation of PDGFRI3 on aerobic glycolysis in osteosarcoma. The results of qPCR and western blot further confirmed the prediction of bioinformatics. Glucose metabolism experiments proved that PDGF/PDGFRI3 could effectively promote aerobic glycolysis in osteosarcoma cells. In addition, the mitochondrial membrane potential (AtIsm) experiment proved that the metabolic change triggered by PDGFRI3 was not caused by mitochondrial damage. The PI3K pathway inhibitor LY294002, MEK pathway inhibitor U0126, or Warburg effect inhibitor DCA was used to perform western blot and glucose metabolism experiments, and the results showed that PDGFBB/PDGFRI3 mainly activated the PI3K/AKT/mTOR/c-Myc pathway to promote aerobic glycolysis in osteosarcoma HOS cells. The newly elucidated role of PDGFRI3 provides a novel metabolic therapeutic target for osteosarcoma.

Automated summary

This study demonstrated that PDGFRI3 has a positive regulatory role in glucose metabolism of osteosarcoma cells, promoting aerobic glycolysis through the activation of the PI3K/AKT/mTOR/c-Myc pathway. This newly discovered role provides a novel metabolic therapeutic target for osteosarcoma.