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. Author manuscript; available in PMC: 2012 Dec 1.
Published in final edited form as: Cancer Res. 2011 Sep 21;71(23):7312–7322. doi: 10.1158/0008-5472.CAN-11-1109

Figure 4. Inhibition of Src activation results in apoptotic cell death.

Figure 4

(A) Flow cytometric and western blot analysis of activated Src shows reduced phospho-Src levels in BaF3 cells stably expressing the three chimeric FGFR1 kinases following Dasatinib treatment. ZNF112 expresses ZMYM2-FGFR1, CEP2A and CEP5A cells express CEP110-FGFR1 and BBC1 expresses BCR-FGFR1. (B) Apoptosis and cell cycle analyses show that Dasatinib treatment (300 nM for ZNF112, CEP2A and CEP5A; 1000 nM for BBC, treated for 48h) remarkably increased cell apoptosis rate and decreased the percentage of cells in the S+G2 phase in ZMYM2-FGFR1 and CEP110-FGFR1 expressing cells. (C) Immunoprecipitation with anti-FRS2 in CEP2A and ZNF112 cells shows that both the phopho-FGFR1 fusion kinase and phospho-Src are present in the same immunocomplex. (D) Flow cytometry analysis shows infection with a dominant negative K295R/Y527F Src (pDNSrc) retroviral construct induces cell death in the cell lines expressing the chimeric FGFR1 kinases compared with the empty vector alone.