Vanadium-rutin complex sensitizes breast cancer cells via modulation of p53/BAx/BCl2/VEGF correlated with apoptotic events

Abstract

In pursuit of a novel approach in breast cancer therapy, we explored the ability of vanadium-rutin complex to eradicate cancer by efficiently targeting various apoptotic pathways on human breast cancer cell lines. We provide direct proof of the chemotherapeutic potential of the vanadium-rutin complex by activating p-53 dependent intrinsic apoptosis and modulating the VEGF pathways. The complex was also capable of binding and cleaving CT-DNA at different concentrations. The complex was able to inhibit cell viability at 100 and 150 µM doses in both MCF7 and MDA-MB-231 cells. Furthermore, the complex successfully initiated apoptosis in both cell lines by activating the p53 dependent intrinsic apoptotic pathway. In vitro studies also established that the complex modulated p53, Bax, Bcl2 and VEGF expressions and induced DNA fragmentation in both the cell lines.