PDGFRB overexpression

This study provides initial evidence that PA, through its interaction with PDGFRB, alters the PI3K/Akt signalling pathway, leading to ferroptosis in gastric cancer cells, thus manifesting its antitumour properties. This discovery holds promise for the development of novel therapeutic strategies for gastric cancer patients.

Our results demonstrated that HIF1A up-regulated PDGFRB under hypoxic conditions, and PDGFRB regulated the actin cytoskeleton, a process likely linked to the activation of RhoA and the phosphorylation of, thereby promoting OS dedifferentiation and pulmonary metastasis.

Finally, we demonstrated that a subset of HCC mouse models that overexpressed PDGFRB -as detected in parallel in human HCC cohorts- could be specifically treated by a receptor tyrosine kinase inhibitor. Overall, our results suggest that proteomic-level alterations not readily observed by genomics represent cancer vulnerabilities that need to be carefully considered as potential targets for personalized treatments.