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Tumor necrosis factor induces apoptosis in hepatoma cells by increasing Ca(2+) release from the endoplasmic reticulum and suppressing Bcl-2 expression.

Authors
Kim, BC; Kim, HT; Mamura, M; Ambudkar, IS; Choi, KS; Kim, SJ
Citation
The Journal of biological chemistry, 277(35):31381-31389, 2002
Journal Title
The Journal of biological chemistry
ISSN
0021-92581083-351X
Abstract
Tumor necrosis factor (TNF) plays an import role in the control of apoptosis. The most well known apoptotic pathway regulated by TNF involves the TNFR1-associated death domain protein, Fas-associated death domain protein, and caspase-8. This study examines the mechanism of TNF-induced apoptosis in FaO rat hepatoma cells. TNF treatment significantly increased the percentage of apoptotic cells. TNF did not activate caspase-8 but activated caspase-3, -10, and -12. The effect of TNF on the expression of different members of the Bcl-2 family in these cells was studied. We observed no detectable changes in the steady-state levels of Bcl-X(L), Bax, and Bid, although TNF suppresses Bcl-2 expression. Dantrolene suppressed the inhibitory effect of TNF on Bcl-2 expression. TNF induced release of Ca(2+) from the endoplasmic reticulum (ER) that was blocked by dantrolene. Importantly, the expression of Bcl-2 blocked TNF-induced apoptosis and decreased TNF-induced Ca(2+) release. These results suggest that TNF induces apoptosis by a mechanism that involves increasing Ca(2+) release from the ER and suppression of Bcl-2 expression.
MeSH terms
AnimalsApoptosis/*physiologyCalcium/*metabolismDantrolene/pharmacologyEndoplasmic Reticulum/drug effects/*metabolismGene Expression Regulation, Neoplastic/*drug effects/physiologyGenes, bcl-2/drug effectsKineticsLiver Neoplasms, Experimental/*metabolism/*pathologyProto-Oncogene Proteins c-bcl-2/*genetics/metabolismRatsTransforming Growth Factor beta/pharmacologyTumor Cells, CulturedTumor Necrosis Factor-alpha/*pharmacologybcl-X Protein
DOI
10.1074/jbc.M203465200
PMID
12077131
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Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
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