Abstract：
:EGF-receptor family members (EGFRs) as well as c-Src are over expressed in approximately 70% of breast cancer, and in most of the tumors c-Src is co-over expressed with at least one of the EGFRs, suggesting that they may interact functionally and play a role in the development and progression of the malignancy. We hypothesize that a small molecule inhibitor of c-Src dasatinib (BMS-354825; Bristol Myers Squibb), exerts its effects on breast cancer cells by modulating EGFR signaling. Indeed, we found that dasatinib causes inhibition of breast cancer cells overexpressing EGFR, HER-2 and HER-3 (MDA-MB-468, SKBR3, MDA-MB-453, and MDA-MB-231) in a dose and time-dependent manner. Dasatinib also stimulated apoptosis in MDA-MB-468 cells, which could be attributed to activation of both caspase-9 and -8 and arrest of the cell cycle at G0/G1 cycle. Furthermore, dasatinib markedly inhibited colony formation, cell invasion, migration and angiogenesis, accompanied by decreased phosphorylation of EGFR and c-Src and their downstream effector molecules Akt and Erks. Our data suggest that dasatinib mediates its action in part through EGFR signaling and could be a potential therapeutic agent for breast cancer.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Nautiyal J,Majumder P,Patel BB,Lee FY,Majumdar APdoi
10.1016/j.canlet.2009.03.035subject
Has Abstractpub_date
2009-10-08 00:00:00pages
143-51issue
2eissn
0304-3835issn
1872-7980pii
S0304-3835(09)00227-4journal_volume
283pub_type
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