The novel phospholipase C activator, m-3M3FBS, induces apoptosis in tumor cells through caspase activation, down-regulation of XIAP and intracellular calcium signaling
- 박종욱; 권택규
- Alternative Author(s)
- Park, Jong Wook; Kwon, Taeg Kyu
- Publication Year
- We investigated the effect of the novel
phospholipase C activator, m-3M3FBS, on the apoptosis of
human renal Caki cancer cells. Treatment with m-3M3FBS
induced apoptosis of Caki cells, which was accompanied
by accumulation of sub-G1 phase and DNA fragmentation.
We found that induction of apoptosis is a common
response of several cancer cell types to m-3M3FBS treatment.
Overexpression of Bcl-2 and c-FLIPs fails to block
m-3M3FBS-induced apoptosis. However, ectopic expression
of XIAP partly inhibits m-3M3FBS-induced apoptosis
in Caki cells. m-3M3FBS-induced apoptosis appeared to
involve the XIAP down-regulation and caspase activation.
m-3M3FBS also induced the expression of a potential
proapoptotic gene, C/EBP homologous protein (CHOP),
however, suppression of CHOP expression by small
interfering RNA did not abrogate the m-3M3FBS-induced
apoptosis. In addition, inhibition of phospholipase C (PLC)
or chelation of intracellular calcium prevented m-3M3FBSinduced
apoptosis in Caki cells, suggesting that the
involvement of PLC pathway and intracellular calcium
signaling on the apoptosis in m-3M3FBS-treated Caki
cells. Collectively, our present results suggest that
m-3M3FBS-induced apoptosis in Caki cells may result
from the activation of caspase, down-regulation of XIAP
and intracellular Ca2+ release pathway and that m-3M3FBS
treatment might overcome the anti-apoptotic effect of Bcl-2
or c-FLIPs in cancer cells.
Keywords Phospholipase C activator m-3M3FBS
Apoptosis Calcium XIAP CHOP
- Authorize & License
- Files in This Item:
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.