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Fig. 7 | Molecular Cancer

Fig. 7

From: Development of a 4-aminopyrazolo[3,4-d]pyrimidine-based dual IGF1R/Src inhibitor as a novel anticancer agent with minimal toxicity

Fig. 7

Schematic diagram to describe the action of LL28. In NSCLC cells, IGF1R and Src mutually activate in a normal state. Blockade of IGF1R by treatment with linsitinib induces the Src-mediated compensation of the IGF1R blockade. Similarly, treatment with dasatinib leads to the IGF1R-mediated compensation of the Src blockade. These overall processes cause drug resistance and maintain cell survival. LL28-induced simultaneous suppression of both IGF1R and Src blocks these feedback activations, thereby inducing apoptotic cell death in NSCLC cells

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