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Fig. 3 | Molecular Cancer

Fig. 3

From: Function of the c-Met receptor tyrosine kinase in carcinogenesis and associated therapeutic opportunities

Fig. 3

Crosstalk between c-Met and EGFR. a, b The tyrosine kinase receptors EGFR and c-Met can initiate downstream PI3K/Akt signaling resulting in anti-apoptotic processes and Grb2/MAPK activation to promote the proliferation of tumor cells. Therefore, it is speculated that there might be an effect that allows c-Met to bypass the EGFR receptor to activate its downstream pathway, resulting in resistance to EGFR-TKI monotherapy. c c-Met-TKI monotherapy triggers upregulation of the EGFR ligand TGF-α, as well as upregulation of the EGFR protein family receptor ErbB3, which can contribute to one of the most potent dimers that can activate c-Met downstream pathways leading to acquired resistance in cancer cells

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