Objective: To explore the effect of Withaferin A on A549 cellular proliferation and apoptosis in non-smallcell lung cancer (NSCLC). Materials and
Methods: NSCLC cell line A549 was selected to explore the effect ofWithaferin A on A549 cellular proliferation, apoptosis and the PI3K/Akt signal pathway capable of regulatingtumor biological behavior by assessment of cellular proliferation, cellular apoptotic rates and cellular cyclingas well as by immuno-blotting.
Results: Withaferin A could inhibit A549 cellular proliferation and the controlrate was dosage-dependent (P<0.05), which also increased time-dependently with the same dosage of WithaferinA (P<0.05). The apoptotic indexes in A549 cells treated with 0, 2.5, 5.0, 10.0 and 20.0 μmol·L-1 Withaferin Afor 48 h were significantly different (P<0.05). In addition, the apoptotic rates of each group in both early andadvanced stages were higher than those in 0 μmol·L-1 (P<0.05), which were evidently higher after 48 h thanthose after 24 h (P<0.05). A549 cells treated by Withaferin A for 48 h were markedly lower in Bcl-2 level andobviously higher in Bax and cleaved caspase-3 levels than those treated by 0 μmol·L-1 Withaferin A (P<0.05), andthere were significant differences among 5, 10 and 20 μmol·L-1 Withaferin A (P<0.05). The ratios of A549 cellstreated by Withaferin A for 48 h in G0/G1 stage were higher than those in 0 μmol·L-1 , while those in S and G2/Mstages were obviously lower than those in G2/M stage, and there were significant differences in 5.0, 10.0 and 20.0μmol·L-1 Withaferin A (P<0.05). Additionally, p-Akt/Akt values were in reverse association with dosage, and thedifferences were significant (P<0.05).
Conclusion: Withaferin A can inhibit the proliferation and apoptosis ofA549 cells by suppressing activation of the PI3K/Akt pathways.