Background: Present investigation evaluates the antitumor activity of epifriedelinol for the management of cervical cancer by inducing process of apoptosis. Methods: Human Cervical Cancer Cell Line, C33A and HeLa were selected for study and treated with epifriedelinol at a concentration of (50-1000 µg/ml). Cytotoxicity of epifriedelinol was estimated by MTT assay and induction of apoptosis was assessed by estimating the activity of caspase 3, 8 and 9 enzyme, apoptosis assay and translocation of cytochrome c. Moreover an expression of several proteins that plays role in the apoptosis process was estimated by western blot method. Results: Result of the study suggested that treatment with epifriedelinol significantly decrease the viability count of cancerous cell in a dose perndent manner and also enhances the formation of oligonucleosome in both the cell lines. However activity of caspase enzymes and translocation of cytochrome c were enhanced after treatment with epifriedelinol. It was also observed that epifriedelinol treatment alters the ratio of pro-apoptotic to anti-apoptotic proteins and enhances the expressions of inhibitor of apoptosis proteins (IAP). Conclusion: Result of our study proves the anticancer activity of epifriedelinol in cervical cancer by inducing apoptosis as treatment with it enhances the production of oligonucleosomes, translocation of cytochrome c and activity caspase enzymes.

Purpose: To investigate the anticancer activity of apigenin on human cervical cancer cells. Methods: The anti-proliferative effects of apigenin on HeLa cervical cancer cells were determined by 3-(4,5-dimethylthiazol-2-yl)-)-2,5-diphenyltetrazolium bromide (MTT) and clonogenic assays, while its effect on apoptosis was assayed by DAPI and annexin V/PI double staining. Expression of proteins was assessed by immunoblotting. Results: Apigenin exerted anticancer effects on HeLa cervical cancer cells with an IC50 of 15 µM, and also reduced the colony formation of HeLa cells. These antiproliferative effects were due to induction of apoptosis as indicated by DAPI and annexin V/PI staining. Apigenin altered Bax/Bcl-2 ratio, thereby triggering apoptosis, and also inhibited the Raf/MEK/ERK signalling pathway. Conclusion: These results indicate that apigenin suppresses the growth of cervical cancer cells and may prove to be an important molecule for the treatment of cervical cancer.