Maedeh Bejary - Department of Biology, Faculty of Science, University of Guilan, Rasht, Iran
Soheila Talesh Sasani - Department of Biology, Faculty of Science, University of Guilan, Rasht, Iran
S Mohsen Asghari - Department of Biology, Faculty of Science, University of Guilan, Rasht, Iran

Breast cancer is the main cause of cancer death in women. Human pp60c-Src (or c-Src) is a 60 kDa non-receptor tyrosine kinase encoded by the Rous sarcoma gene (Src). C-Src functions in several signal transduction cascades that affect cellular proliferation, motility, differentiation, survival and regulate blood vessels growth. Tyrosine phosphorylation of VEGF receptor1 (VEGFR1) facilitates binding to the Src homologue domain. Inhibition of vascular endothelial growth factor (VEGF) binding to its receptor increases the efficiency of chemotherapy. In this study we will assess c-Src expression level in Balb/c mice (pasteur institute, Iran) having 4T1 cell-line induced and were treated with a VEGFB antagonist peptide. Breast tissue samples were obtained from treated and untreated mice (as control). Total RNA was isolated using Trizol reagent(Invitrogen) followed by cDNA synthesis. Real time polymerase chain reaction was carried out using c-Src specific primers and relative expression of c-Src gene was assessed. We used U6 gene as the reference. Our results showed the expression level of c-Src gene was different between treated group and control. The results suggest that Src inhibition may be a useful drug target for angiogenesis suppression.

Angiogenesis; VEGFR1; c-Src; Cancer