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Fig. 6 | Molecular Cancer

Fig. 6

From: Targeting the insulin-like growth factor receptor and Src signaling network for the treatment of non-small cell lung cancer

Fig. 6

Schematic model of the IGF-IR TKI resistance. (a) Src, a common downstream node of various membrane-associated receptors, stimulates downstream signaling molecules. (b) IGF-1R and Src are simultaneously co-activated through mutual phosphorylation in human NSCLCs. The suppression of IGF-1R with a TKI reprograms high- pSrc-expressing NSCLC cells to stimulate downstream signaling effectors via alternative pathways of Src activation through various plasma membrane-associated receptors resulting in drug resistance. (c) The IGF-1R TKI-mediated suppression of IGF-1R in low-pSrc-expressing NSCLC cells induces the posttranslational reprogramming of the cellular machinery to decrease the turnover of the IGF-1R and Src proteins, which in turn augments reciprocal co-activation of Src and IGF-1R, resulting in drug resistance

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