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Comparison of the anti‐apoptotic effects of Bcr‐Abl, Bcl‐2 and Bcl‐x L following diverse apoptogenic stimuli
Author(s) -
Brumatti Gabriela,
Weinlich Ricardo,
Chehab Cristina F,
Yon Monica,
Amarante-Mendes Gustavo P
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)00299-0
Subject(s) - xiap , apoptosis , chemistry , cancer research , cytochrome c , breakpoint cluster region , ectopic expression , microbiology and biotechnology , biology , programmed cell death , cell culture , caspase , biochemistry , genetics , receptor
Ectopic expression of Bcr‐Abl, Bcl‐2 or Bcl‐x L in HL‐60 cells conferred resistance to apoptosis against a variety of death‐inducing agents. Bcr‐Abl‐mediated interference with mitochondrial events was confirmed by the analysis of the loss of mitochondrial transmembrane potential and cytochrome c release. HL‐60.Bcr‐Abl cells were extremely resistant to all apoptogenic stimuli tested, even in circumstances where HL‐60.Bcl‐2 or HL‐60.Bcl‐x L cells were only partially protected from apoptosis. The levels of Mcl‐1, Bax, Bid, Akt, c‐IAP‐1, c‐IAP‐2, XIAP and c‐FLIP were compared in all HL‐60 lines. Our findings show that Bcr‐Abl is a more powerful anti‐apoptotic molecule than Bcl‐2 or Bcl‐x L .