Poster Abstract


January 8, 2010

Bang!! and the Cancer Cell Dies

Wayne Warner
MARC U*STAR Fellow
Summer Research Site: St Jude Children’s Research Hospital Memphis TN

One of the hallmarks of tumorigenesis is the ability of cancer cells to evade apoptosis. The over-expression of BCL-XL is a common mechanism that allows cells to evade the signals that lead to programmed cell death. This pro survival BCL2 family member binds and inhibits the pro-apoptopic Bax and Bak. A previous study had shown that a small molecule bang-52 down-regulated BCL-XL in a lymphoblast derived cell line, TK6, and induced apoptosis by a novel mechanism. This current study shows an up-regulation of BCL-XL, Mcl1, and an induction of apoptosis under similar conditions. While these findings contradict the results of the previous study they nevertheless point to Bang 52 as a viable therapeutic agent for induction of apoptosis in lymphoma cell lines and worthy of future study.  

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