In the in vitro study, the conjugate presented a great cytolytic activity in DU 145 prostate cancer cells and SK-OV ovarian cancer cells that exhibited high MMP-2 activity. Besides, the conjugate showed low cytotoxicity in normal cells with selleck chemical low MMP-2 activity in vitro. In vivo, the tumors injected with the complex melittin/avidin were maintained with a smaller size

comparing to non-treated tumors, indicating the great potential of this treatment in the fight against cancer. Ling et al. (2004) built a recombinant adenovirus carrying the melittin gene and α-fetoprotein (AFP) promoter (Ad-rAFP-Mel). It has been shown that the melittin mRNA was transcribed in HepG2 hepatocellular carcinoma cells transduced by AdrAFP-Mel. The tumorigenicity rates of hepatocarcinoma cells transfected with Ad-rAFP-Mel were lower comparing with non-transfected cells. A significant antineoplastic effect was detected in the transplanted tumor in nude mice after an intratumoral injection

of Ad-rAFP-Mel. Ling et al. (2005) also reported lower tumorigenicity rates of hepatocarcinoma cells transfected with Ad-rAFP-Mel. A significant antineoplastic effect was detected on the transplanted tumor in nude mice after an intratumoral injection of Ad-rAFP-Mel. Li et al. (2006) further showed that an AdrAFP-Mel infection markedly induces cellular apoptosis, and Fas expression on Bel-7402 cells. They suggested this to be a possible molecular mechanism KU-57788 solubility dmso for the antitumorigenecity of AdrAFP-Mel even though more studies will be needed. In an in vivo study, Orsolic et al. (2003) showed that, when intravenously injected, BV significantly Cediranib (AZD2171) inhibited mammary carcinoma metastasis (P < 0.001)

in mice injected also intravenously with this type of tumor, when compared to control mice. However, when the venom was subcutaneously administered, no differences in metastasis formation were observed. The tumor also decreased in size when the venom was administered intratumorally, and mice survived longer than control, indicating that the in vivo venom action depends on how the venom is injected. Jang et al. (2003) studied the effects of BV in NCI-H1299 lung cancer cells and verified that cells treated with 10 μg/ml of venom for 24 h exhibited morphological changes typical of apoptotic cells, which was confirmed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, DAPI staining assay and DNA fragmentation detected via agarose electrophoresis. Furthermore, flow cytometric analyses showed an accumulation of cells in the sub G1 phase of cell cycle in treated cells compared to control. It was also demonstrated that BV treatment resulted in an increase in the expression of Bax, a pro-apoptotic protein, and a decrease in the expression of Bcl-2, a protein that heterodimerizes with Bax, suppressing cell death.