Flavonoids As Inhibitors or Enhancers of the Cytotoxicity of Tumor Necrosis Factor-α in L-929 Tumor Cells

1997 ◽  
Vol 60 (8) ◽  
pp. 775-778 ◽  
Author(s):  
Solomon Habtemariam
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Endogenous Bak inhibitors Mcl-1 and Bcl-xL: differential impact on TRAIL resistance in Bax-deficient carcinoma

2010 ◽  
Vol 188 (6) ◽  
pp. 851-862 ◽  
Author(s):  
Bernhard Gillissen ◽  
Jana Wendt ◽  
Antje Richter ◽  
Anja Richter ◽  
Annika Müer ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Death Receptor ◽  
Apoptosis Pathway ◽  
Mitochondrial Apoptosis Pathway ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

Tumor necrosis factor (α)–related apoptosis-inducing ligand (TRAIL) is a promising anticancer agent that preferentially kills tumor cells with limited cytotoxicity to nonmalignant cells. However, signaling from death receptors requires amplification via the mitochondrial apoptosis pathway (type II) in the majority of tumor cells. Thus, TRAIL-induced cell death entirely depends on the proapoptotic Bcl-2 family member Bax, which is often lost as a result of epigenetic inactivation or mutations. Consequently, Bax deficiency confers resistance against TRAIL-induced apoptosis. Despite expression of Bak, Bax-deficient cells are resistant to TRAIL-induced apoptosis. In this study, we show that the Bax dependency of TRAIL-induced apoptosis is determined by Mcl-1 but not Bcl-xL. Both are antiapoptotic Bcl-2 family proteins that keep Bak in check. Nevertheless, knockdown of Mcl-1 but not Bcl-xL overcame resistance to TRAIL, CD95/FasL and tumor necrosis factor (α) death receptor ligation in Bax-deficient cells, and enabled TRAIL to activate Bak, indicating that Mcl-1 rather than Bcl-xL is a major target for sensitization of Bax-deficient tumors for death receptor–induced apoptosis via the Bak pathway.

scholarly journals PG490 (Triptolide) Cooperates with Tumor Necrosis Factor-α to Induce Apoptosis in Tumor Cells

1999 ◽  
Vol 274 (19) ◽  
pp. 13451-13455 ◽  
Author(s):  
Kye Young Lee ◽  
Wen-teh Chang ◽  
Daoming Qiu ◽  
Peter N. Kao ◽  
Glenn D. Rosen
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor
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