Thus our data illustrated that phosphorylation of GSK3[beta] and hence inactivation of this protein together with the presence of cleaved caspase-8 and -3 was due to Lanatoside C's induction of extrinsic apoptotic pathway in epithelial like liver cancer cell Huh7 through JNK1 activation (Fig.
lanatoside C, and Glucogitoroside or DMSO controls for 24 h representing G2-M arrest in treated cells.
However, whether Cardiac glycoside Lanatoside C can induce oxidative stress in liver cancer cells and induce cell death both in vitro and in vivo remains unknown.
Results: In this study, we found that Cardiac glycosides, particularly Lanatoside C from Digitalis ferruginea could significantly inhibit PTEN protein adequate Huh7 and PTEN deficient Mahlavu human liver cancer cell proliferation by the induction of apoptosis and G2/M arrest in the cells.
Conclusion: The results indicated that Lanatoside C could be contemplated in liver cancer therapeutics, particularly in PTEN deficient tumors.
This study investigates the antitumor activity of cardiac glycosides, particularly Lanatoside C, in liver cancer cells both in vitro and in vivo.
Initial and majority of in vitro experiments were done with pure Lanatoside C (D.
Then 2 [micro]M Lanatoside C (L2261, Sigma Aldrich) was applied to the cells.
Control group mice (5 mice) received only simple syrup and other subjects received 6 mg/kg Lanatoside C (8 mice) in simple syrup by gavage feeding (5 days/week).
The cardiac glycosides Lanatoside A, Lanatoside C and Glucogitoroside showed significant levels of cytotoxicity whereas the phenylpropanoid glycosides had no notable effects on cell growth (Fig.
An increase in the G2/M phase was observed in cells treated with Lanatoside A, Lanatoside C and Glucogitoroside compared to cells in the DMSO controls (Fig.