IGF-1R And PDGFR? In Glioma Cells Interaction And Function Studies

Objective: The TCGA database revealed that IGF-1R is most significantly correlated with PDGFRA expression,and dual targeting of IGF-1R and PDGFR can more effectively inhibit the growth of glioma cells.This study intends to investigate the possible interaction and function of IGF-1R and PDGFR? in glioma cells.Methods:(1)Analysis of the TCGA database revealed the correlation between PDGFRA and other RTK expressions.(2)CO-IP technology detects the interaction between IGF-1R and PDGFR? in OPC-like glioma cells.(3)IGF-1 and PDGFAA respectively treat OPC-like glioma cells,and Western Blot technology was used to detect the phosphorylation degree of IGF-1R and PDGFR?.(4)IGF-1 and PDGFAA treated OPC-like glioma cells separately,and RT-q PCR technology was used to detect the m RNA expression level of IGF-1.(5)IGF-1 and PDGFAA were used to treat patients' GBM glioma cells.Western Blot technology was used to detect the phosphorylation degree of IGF-1R and PDGFR?.Results:(1)The correlation between IGF-1R and PDGFRA expression was most obvious in TCGA.(2)The Co-immunoprecipitation results show that the interaction of IGF-1R and PDGFR? in OPC-like glioma cells.(3)The Western Blotting results show that the functional interaction between IGF-1R and PDGFR? in OPC-like glioma cells.(4)The q PCR results show that PDGFAA stimulated OPC-like glioma cells to promote IGF-1 m RNA expression.(5)The Western Blotting results show that the functional interaction between IGF-1R and PDGFR? in patients GBM cells.Conclusion:(1)There are interactions of IGF-1R and PDGFR? in glioma.(2)IGF-1 stimulates glioma cells to cause IGF-1R phosphorylation,and at the same time can rapidly activate PDGFR? phosphorylation.(3)PDGFAA stimulates glioma cells to cause PDGFR? phosphorylation,and promotes the increase of IGF-1 m RNA expression.(4)In patients' GBM cells,IGF-1 stimulates glioma cells to promote IGF-1R phosphorylation and PDGFR? phosphorylation;PDGFAA stimulates patient's GBM cells to cause IGF-1R and PDGFR? phosphorylation.