Anti- @entity5 effect of XXXX venom on @entity694 cell growth by activation of death receptors and inhibition of nuclear factor kappa B.

@entity627 @entity625 @entity5 @entity73322 @entity158 @entity272 @entity73321 @entity694 @entity5157
UNASSIGNED: @entity5157 venom (BV) has been used as a traditional medicine to treat @entity625 , @entity627 , back @entity158 , @entity5 , and @entity272 . However, the effects of BV on the @entity694 and their action mechanisms have not been reported yet. We used cell viability assay and soft agar colony formation assay for testing cell viability, electro mobility shift assay for detecting DNA binding activity of nuclear factor kappa B (NF-kB) and Western blotting assay for detection of apoptosis regulatory proteins. We found that BV inhibited growth of @entity694 cells through induction of apoptosis. We also found that the expression of death receptor (DR) 4, DR5, p53, p21, Bax, cleaved caspase-3, cleaved caspase-8, and cleaved caspase-9 was increased by BV treatment in a dose dependent manner (0-5  g/ml). Consistent with @entity5 cell growth inhibition, the DNA binding activity of nuclear factor kappa B (NF-kB) was also inhibited by BV treatment. Besides, we found that BV blocked NF-kB activation by directly binding to NF-kB @entity73321 subunit. Moreover, combination treatment with BV and @entity73321 siRNA or NF-kB inhibitor augmented BV-induced cell growth inhibition. However, @entity73321 mutant plasmid ( @entity73322 ) transfection partially abolished BV-induced cell growth inhibiton. In addition, BV significantly suppressed @entity5 growth in vivo. Therefore, these results suggested that BV could inhibit @entity694 cell growth, and these anti-proliferative effects may be related to the induction of apoptosis by activation of DR4 and DR5 and inhibition of NF-kB.
