Influence of Gold Nanoparticle Tagged Snake Venom Protein Toxin NKCT1 on Ehrlich Ascites Carcinoma (EAC) and EAC Induced Solid Tumor Bearing Male Albino Mice
Partha Pratim Saha,
Anjan Kumar DasGupta,
Earlier the conjugation of gold nanoparticle (GNP) and snake venom protein toxin NKCT1 was reported and
primary characterization was performed. In the present communication, further characterizations of GNP-NKCT1 were
done with SEM, EDS, XRD and Raman spectra for its physio-chemical nature and bonding. SEM showed the formation
of gold nanoparticles, whereas EDS and XRD confirmed 60-90% gold nanoparticles in the solution. Raman shift corresponding
to (C=O), (N-H), (C-N) confirmed the proper conjugation of GNP with NKCT1. GNP-NKCT1 showed anticancer
effect both in vivo and in vitro in EAC cell and antitumor effect in EAC induced mice. In in vivo studies, GNPNKCT1
increased MST 108.30% and decreased viable EAC cell count 51.39%. Fluorescent micrograph showed signs of
apoptosis (membrane blebbing, membrane disruption). Decreased level of IL-10 and low incorporation of BrdU showed
decreased proliferation of EAC induced by GNP-NKCT1. With upregulation of Bax, down regulation of Bcl2 and increased
expression of caspase 3/9, it was confirmed that GNP-NKCT1 induced caspase dependent apoptosis pathway in
EAC cell. In in vitro studies, GNP-NKCT1 increased the late apoptotic stage of cell and arrested cell cycle division at
G0/G1 state. GNP-NKCT1 also decreased the tumor volume and tumor weight in EAC induced tumor in male albino mice.
It inhibited angiogenesis, which was confirmed by lower percentage of expression of VEGF. This study indicated the capability
of gold nanoparticles which enhanced the tumor uptake of NKCT1 and also suggested that GNP-NKCT1 might
be a good source for anti-carcinoma and anti-tumor agents.
Keywords: Apoptosis, Caspase, Ehrlich ascites carcinoma, Gold nanoparticle, Snake venom, Tumor.
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