作者: X Wu , Z Fan , H Masui , N Rosen , J Mendelsohn
DOI: 10.1172/JCI117871
关键词:
摘要: Both EGF and insulin, or IGF, stimulate the growth of many cell types by activating receptors that contain tyrosine kinase activities. A monoclonal antibody (mAb 225) against receptor produced in this laboratory has been shown to competitively inhibit binding block activation kinase. Here we report a human colorectal carcinoma line, DiFi, which expresses high levels on plasma membranes, can be induced undergo G1 cycle arrest programmed death (apoptosis) when cultured with mAb 225 at concentrations saturate receptors. Addition IGF-1 insulin delay apoptosis 225, while cannot reversed either insulin. Insulin/IGF-1 activate inhibited 225. Moreover, an receptor, little direct effect DiFi growth, capacity insulin/IGF-1 suggesting insulin/IGF-1-mediated is acting through receptor. In contrast, caused DNA damaging agent, cisplatin. The results indicate required both for progression prevention cells, signal transduction pathway shared may involved regulating triggered blockade