A role for the subcellular localization of Bax in differentiation-induced resistance to apoptosis in HL-60 cells.
The promyelocytic leukemia cell line HL-60 was induced to undergo granulocytic differentiation by treatment with dimethyl sulphoxide (DMSO). The differentiated HL-60 cells were resistant to apoptosis induction by etoposide treatment. The resistant cells did not show evidence of cytochrome c release from the mitochondria or cleavage of caspase-3. Because of the important role of Bax in the regulation of apoptosis in HL-60 cells and neutrophils, we studied its levels and sub-cellular localization in susceptible and resistant HL-60 cells. Although, there was no significant change in Bax levels as a result of DMSO treatment, resistance to apoptosis was associated with lack of Bax translocation from the cytosol to the mitochondria-containing fraction. These results emphasize the role of Bax in apoptosis and point out the importance of studying not only its level, but also its sub-cellular localization.[1]References
- A role for the subcellular localization of Bax in differentiation-induced resistance to apoptosis in HL-60 cells. Abdelhaleem, M. Anticancer Res. (2002) [Pubmed]
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