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OBJECTIVE: Homeopathic nosodes have seldom been scientifically validated for their anticancer effects. This study was conducted to examine if a recently developed hepatitis C nosode has demonstrable anticancer potential in cancer cells in vitro.METHODS: Anticancer effects of Hepatitis C 30C(Hep C 30), if any, were initially tested on three cancer cell lines, HepG2(liver cancer), MCF-7(breast cancer) and A549(lung cancer) and one normal liver cell line WRL-68 cells and subsequently a more thorough study using further scientific protocols was undertaken on HepG2 cells(against WRL-68 cells as the normal control) as HepG2 cells showed better anticancer response than the other two. Three doses, one at 50% lethal dose(LD_(50)) and the other two below LD_(50), were used on HepG2 cells subsequently. Protocols like apoptosis induction and its possible signaling mechanism were deployed using immunoblots of relevant signal proteins and confocal microscopy, with particular reference to telomerase and topoisomerase Ⅱ(Top Ⅱ) activities, two strong cancer biomarkers for their direct relationship with divisional activities of cells and DNAs. RESULTS: Hep C 30 induced apoptosis, caused distorted cell morphology typical of apoptotic cells, increased reactive oxygen species generation and produced increased DNA nicks. Further it enhanced pro-apototic signal proteins like Bax, cytochrome c and inhibited anti-apoptotic signal proteins, Bcl-2, cytochrome c and caspase-3, changed mitochondrial membrane potential and caused externalization of phosphatidylserine. The drug also decreased expression of two cancer biomarkers, Top Ⅱ and telomerase, consistent with its anticancer effect. CONCLUSION: Hep C 30 has demonstrable anticancer effects against liver cancer cells in vitro.
OBJECTIVE: Homeopathic nosodes have seldom been scientifically validated for their anticancer effects. This study was undertaking to examine if a recently developed hepatitis C nosode has demonstrable anticancer potential in cancer cells in vitro. METHODS: Anticancer effects of Hepatitis C 30C (Hep C 30) , if any, were initially tested on three cancer cell lines, HepG2 (liver cancer), MCF-7 (breast cancer) and A549 (lung cancer) and one normal liver cell line WRL-68 cells and subsequently a more thorough study using further Three protocols, one at 50% lethal dose (LD_ (50)) and the other two below Protocols like apoptosis induction and its possible signaling mechanism were deployed using immunoblots of relevant signal proteins and confocal microscopy, with particular reference to telomerase and topoisomerase Ⅱ (Top Ⅱ) activities, two strong cancer biomarkers for their direct relationship with divisional activities of cells and DNAs. RESULTS: Hep C 30 induced apoptosis, caused distorted cell morphology typically apoptotic cells, increased reactive oxygen species generation and increased production DNA nicks. Further it enhanced pro-apototic signal proteins like Bax, cytochrome c and inhibited anti-apoptotic signal proteins, Bcl-2, cytochrome c and caspase-3, changed mitochondrial membrane potential and caused externalization of phosphatidylserine. The drug also decreased expression of two cancer biomarkers, Top II and telomerase, consistent with its anticancer effect. CONCLUSION: Hep C 30 has demonstrable anticancer effects against liver cancer cells in vitro.