Journal
FORSCHENDE KOMPLEMENTARMEDIZIN
Volume 22, Issue 3, Pages 172-179Publisher
KARGER
DOI: 10.1159/000433485
Keywords
DNA methylation; CpG islands; Epigenetic modification; Condurango 30C; Lung cancer; PCR-SSCP analysis; Homeopathy
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Funding
- Department of Zoology, University of Kalyani
- Boiron Laboratory, Lyon, France
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Background: DNA hypermethylation induces cancer progression involving CpG island of DNA and causes inactivation of tumour suppressor genes. In this study, DNA hypermethylation status of lung cancer and ability of ultra-highly diluted Condurango 30C to modulate DNA methylation were ascertained by analysis of lung cancer-specific tumour suppressor genes in respect to placebo. Materials and Methods: DNA methylation status, if any, was determined by PCR-SSCP analyses in lung cancer-specific tumour suppressor genes (p15, p16 and p53) using H460-NSCLC cell and BaP-induced lung cancer of rats. The ability of Condurango 30C to modulate DNA methylation, if any, was verified against placebo control in blinded manner. Results: Condurango 30C-treated DNA showed significant decrease in band intensity of p15 and p53 genes especially in methylated condition in vitro, at IC50 dose (2.43 mu l/100 mu l). SSCP analysis of p15 and p53 genes in Condurango 30C-treated DNA also suggests that Condurango 30C can decrease methylation, in vitro. Inhibition of p15 hypermethylation was observed in post-cancer treatment of rats with Condurango 30C. SSCP results gave a better indication of differences in band position of p15 and p53 in Condurango 30C-treated lung samples. Conclusion: Condurango 30C could trigger epigenetic modification in lung cancer via modulation of DNA hypermethylation.
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