Bcl-2 completely blocks Fas-mediated apoptosis in mtDNA-depleted HeLa cells.
Bcl-2 inhibits apoptosis induced by a variety of death stimuli but does not completely inhibit Fas-mediated apoptosis. We have previously shown that a HeLa-derived cell line lacking mitochondrial DNA (mtDNA) expresses Fas at a high level and apoptosis is easily induced using a low concentration of an anti-Fas antibody. In this study, overexpression of Bcl-2 in the mtDNA-less cells completely blocked Fas-mediated apoptosis, and this was not due to a depression of the enhanced Fas expression. These findings suggest that the Fas-mediated apoptotic pathway is directly linked to Bcl-2 protection in the cells with an accompanying mitochondrial dysfunction.
Asoh
S
S
Department of Biochemistry and Cell Biology, Nippon Medical School, Kanagawa, Japan.
Ohta
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S
D000906:Antibodies / Q000633:toxicity; D017209:Apoptosis / Q000502:physiology*; D002470:Cell Survival; D004272:DNA, Mitochondrial / Q000235:genetics / Q000378:metabolism*; D005434:Flow Cytometry; D006367:HeLa Cells; D006801:Humans; D016133:Polymerase Chain Reaction; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis / Q000502:physiology*; D011994:Recombinant Proteins / Q000096:biosynthesis / Q000378:metabolism; D014162:Transfection; D019014:fas Receptor / Q000276:immunology / Q000502:physiology*
D000906:Antibodies; D004272:DNA, Mitochondrial; D019253:Proto-Oncogene Proteins c-bcl-2; D011994:Recombinant Proteins; D019014:fas Receptor