Inhibition of viral oncogenesis as well as adjuvant role of herbal extracts in cancer

Abstract

Cancer is a clonal disorder and is genetically thought to be the results of multiple genetic events. Despite recent advances in our understanding of the biological processes leading to the development of cancer, there is still a need for new and effective agents to bring cancer under control. Some of the chemotherapeutic agents which are currently in clinical use such as camptothecin, taxol, etoposide and vinca alkaloids are derived from plants. In the present study we had evaluated the possible biological effects of Berberine, Picroliv, Curcumin, and Phyllanthus amarus against cancer. Friend virus induced erythroleukemia is a useful model to study the viral etiology of cancer and also to find out the drugs that can inhibit viral carcinogenesis. Using this model we have studied the effect of these compounds on the viral carcinogenesis in BALB/c mice. The effect of these compounds on the inhibition of Friend Virus (FMuLv) induced murine erythroleukemia was evaluated in BALB/c mice. These compounds were found to suppress the progression of leukemia as evident from the analysis of hematological and biochemical parameters, histopathological evaluations and expression analysis of selected genes such as Bcl-2, p53, p45NFE2, Raf-1, Erk-1, IFN-gamma receptor and erythropoietin. We also evaluated the antiviral activity of Berberine, Picroliv, Curcumin, and Phyllanthus amarus against Newcastle Disease Virus and Egg Drop Syndrome 76 virus in embryonated eggs and against Poliovirus in Vero cell line in culture. All these compounds were found to have significant antiviral activity against the viruses tested. Tumor cells are often found to be resistant towards apoptosis. The possible apoptotic inducing activity of P.amarus was evaluated in Dalton s Lymphoma Ascites (DLA) cell line and in HepG2 cell lines. P.amarus was found to induce apoptosis in DLA cells and the mechanism by which it induces apoptosis was by the induction of the caspases 3 and inhibiting Bcl- 2 expression.