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- Title
Inhibition of nuclear factor-κB activation is essential for membrane-associated TNF-α-induced apoptosis in HL-60 cells.
- Authors
Wenfang Shi; Lingyun Li; Xu Shi; Fang Zheng; Jingyang Zeng; Xiaodan Jiang; Feili Gong; Muxiang Zhou; Zhuoya Li
- Abstract
The killing of tumour cells that are resistant to soluble TNF-α (sTNF-α) by the membrane-bound form of TNF-α (mTNF-α) suggests that different intracellular signalling pathways are involved. We found that mTNF-α induced apoptosis in HL-60 cells and failed to cause degradation of inhibitor of kappa B alpha (IκB-α) and translocation and activation of nuclear factor kappa B (NF-κB), whereas sTNF-α failed to induce apoptosis, but lowered cytoplasmic inhibitor of kappa B alpha, induced translocation of NF-κB to the nucleus and experimentally increased activity of the regulated luciferase. Furthermore, mTNF-α upregulated the expression of TNF receptor associated factor (TRAF) 1 and failed to induce TRAF1 and TRAF2 membrane translocation, but led to cytoplasmic colocalization. In contrast, sTNF-α stimulated the expression of TRAF1 and TRAF2, recruiting both molecules onto the cell membrane poststimulation. These results suggest that the increased susceptibility of HL-60 cells to mTNF-α may be due to the failure of TRAF2 membrane translocation caused by the upregulation of TRAF1 expression and formation of a TRAF1/TRAF2 complex in the cytoplasm, thereby inhibiting NF-κB activation and inducing apoptosis.
- Subjects
APOPTOSIS; CELL death; CELLS; NF-kappa B; DNA-binding proteins; PROTEIN binding; TRANSCRIPTION factors
- Publication
Immunology & Cell Biology, 2006, Vol 84, Issue 4, p366
- ISSN
0818-9641
- Publication type
Article
- DOI
10.1111/j.1440-1711.2006.01436.x