The effect of non-contact electro capacitive cancer therapy on VEGFR2 expression in DMBA-induced rat breast tumor model Endah Sri Palupi (a), Bambang Retnoaji (b), Pudji Astuti (c), Firman Alamsyah (d), Rarastoeti Pratiwi (e*)
a) Postgraduate Program, Faculty of Biology, Universitas Gadjah Mada
b) Animal Structure and Development Laboratory, Faculty of Biology, Universitas Gadjah Mada
c) Department of Physiology, Faculty of Veterinary, Universitas Gadjah Mada
d) Center for Medical Physics and Cancer Research, Ctech Labs Edwar Technology, Tangerang
e*) Biochemistry Laboratory, Faculty of Biology, Universitas Gadjah Mada
* rarastp[at]ugm.ac.id
Abstract
Angiogenesis contributes to tumor growth and requires signal transduction. VEGFR2 is the primary receptor for the growth factors during tumor angiogenesis. Electro Capacitive Cancer Therapy (ECCT) is an anti-tumor device to inhibit tumor growth. However, its effect on VEGFR2 expression during breast tumor angiogenesis is unclear. Twenty-four rats were divided into 4 groups. Two groups of DMBA-induced rats, while the others were not, with and without ECCT exposure for each. ECCT 150 kHz and 18 Vpp of the AC source were exposed. Mammary glands and breast tumor tissue were collected and preserved. VEGFR2 mRNA expression was measured using qPCR and analyzed using the Livak method with GAPDH normalization. Immunohistochemistry staining was performed on paraffin sections using anti-VEGFR2. The data were statistically analyzed using an independent t-test. The results show that ECCT exposure has no impact on VEGFR2 mRNA expression of normal breast tissue. Insignificant downregulation was expressed in rat breast tumors, in contrast with the ECCT-therapied rat breast tumor. Furthermore, ECCT exposure increased VEGFR2 protein expression significantly, as well as the number of blood vessels. It suggests other mechanisms may be involved in signal transduction during DMBA-induced rat breast tumor angiogenesis.
Keywords: angiogenesis- breast tumor- DMBA- ECCT exposure- VEGFR2
