The inhibitory potency of peptides derived from autophosphorylation sites of receptor tyrosine kinase in a non-ATP-competitive mechanism on tumor cells.

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Previously, based on amino-acid sequences of autophosphorylation sites of receptor tyrosine kinase such as EGFR and IR, we designed small peptides which inhibit phosphorylation of EGFR or IR effectively. The aim of this study was to observe the effects of these peptides on tumor cells. We found that membrane-permeable synthetic peptides derived from EGF receptor autophosphorylation sites have the potential to suppress EGF receptor function in A549 cells and derived from IGF-1 receptor autophosphorylation sites have the potential to suppress IGF-1 receptor function in MCF-7 cells. These peptides have the potential to be developed into novel and useful agents for cancer therapy.