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

在此之前，我们根据受体酪氨酸激酶如EGFR和IR的自磷酸化位点的氨基酸序列，设计了能有效抑制EGFR或IR磷酸化的小肽。本研究的目的是观察这些肽对肿瘤细胞的作用。我们发现，来源于EGF受体自磷酸化位点的膜渗透性合成肽具有抑制A549细胞中EGF受体功能的潜力，而来源于IGF-1受体自磷酸化位点的合成肽具有抑制MCF-7细胞中IGF-1受体功能的潜力。这些多肽有潜力开发成新的和有用的药物用于癌症治疗。

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.