TRAIL-Induced Apoptosis in Type I Leukemic Cells Is Not Enhanced by Overexpression of Bax

Authors: Jia L.; Patwari Y.; Kelsey S.M.; Newland A.C.

Source: Biochemical and Biophysical Research Communications, Volume 283, Number 5, May 2001 , pp. 1037-1045(9)

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Abstract:

We have previously shown that Bax translocation was crucial in TNF alpha or etoposide-induced apoptosis. Overexpression of Bax sensitized chronic myeloid leukemic K562 cells to etoposide-induced apoptosis. Treatment with TNF-related apoptosis-inducing ligand (TRAIL) induces a loss of mitochondrial membrane potential ( Delta Psi m), cytochrome c release from mitochondria, activation of caspases-8, -9, and -3, and cleavage of Bid in the K562 cell line. Bax failed to sensitize K562 cells to TRAIL-induced apoptosis. TRAIL did not induce Bax expression and/or translocation from cytosol to mitochondria in the K562 cell line. However, 100 M Z-VAD.fmk, a pan caspase inhibitor, completely blocked TRAIL-initiated mitochondrial alterations and cleavages of caspases and Bid. We propose that TRAIL-induced apoptosis in K562 cells is via Type I apoptotic signal pathway. Bax translocation is not essential for TRAIL-induced cytochrome c release and Delta Psi m collapse in the Type I cells. Copyright 2001 Academic Press.

Keywords: apoptosis; Bax; caspases; cytochrome c; TRAIL

Language: English

Document Type: Research article

Affiliations: Department of Haematology/Oncology, St. Bartholomew's and The Royal London School of Medicine and Dentistry, Turner Street, London, E1 2AD, United Kingdom

Publication date: 2001-05-01