However, drugs targeting this pathway have shown mixed results in clinical trials, and the detailed mechanisms of how the insulin signaling pathway promotes glioblastoma growth remain to be elucidated.

This study offers an explanation for the difficulties encountered by current drugs targeting IGFIR to reduce glioblastoma cell growth: a secondary mechanism that upregulates HIFloc.

In sum, we have found a possible target in the insulin signaling system that merits exploration as a candidate drug target for glioblastoma patients and other patients with cancers sensitive to the insulin signaling pathway.

To simulate the effect of using different drug targeting factors in glioblastoma, we set each rate constant to 0 separately, modeling the effects of removing each interaction, with the exception of the basal production and degradation of HIFloc.