Human urokinase receptor expression is inhibited by amiloride and induced by tumor necrosis factor and phorbol ester in colon cancer cells

FEBS Letters ◽  
1994 ◽  
Vol 353 (2) ◽  
pp. 138-142 ◽  
Author(s):  
Yao Wang ◽  
Caroline J. Jones ◽  
Jinjun Dang ◽  
Xiaoming Liang ◽  
Jane E. Olsen ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Phorbol Ester ◽  
Tumor Necrosis ◽  
Urokinase Receptor ◽  
Receptor Expression ◽  
Colon Cancer Cells ◽  
Necrosis Factor

scholarly journals Cytokine Induction of Tumor Necrosis Factor Receptor 2 Is Mediated by STAT3 in Colon Cancer Cells

2011 ◽  
Vol 9 (12) ◽  
pp. 1718-1731 ◽  
Author(s):  
Kathryn E. Hamilton ◽  
James G. Simmons ◽  
Shengli Ding ◽  
Laurianne Van Landeghem ◽  
P. Kay Lund
Keyword(s):  
Colon Cancer ◽  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Colon Cancer Cells ◽  
Cytokine Induction ◽  
Necrosis Factor

scholarly journals β-Catenin–dependent lysosomal targeting of internalized tumor necrosis factor-α suppresses caspase-8 activation in apoptosis-resistant colon cancer cells

2013 ◽  
Vol 24 (4) ◽  
pp. 465-473 ◽  
Author(s):  
Jinbo Han ◽  
Priya Sridevi ◽  
Michael Ramirez ◽  
Kirsten J. Ludwig ◽  
Jean Y. J. Wang
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Caspase 8 ◽  
Endosomal Trafficking ◽  
Colon Cancer Cells ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

The Wnt/β-catenin pathway is constitutively activated in more than 90% of human colorectal cancer. Activated β-catenin stimulates cell proliferation and survival, however, its antiapoptotic mechanisms are not fully understood. We show here that activated β-catenin is required to suppress caspase-8 activation, but only in colon cancer cells that are resistant to tumor necrosis factor-α (TNF)-induced apoptosis. We found that lysosomal delivery of internalized TNF occurred at a faster pace in apoptosis-resistant than in apoptosis-sensitive colon cancer cells. Retardation of endosomal trafficking through vacuolar ATPase (V-ATPase) inhibition enhanced caspase-8 activation in apoptosis-resistant but not apoptosis-sensitive cells. Interestingly, knockdown of β-catenin also prolonged TNF association with the early endosome and enhanced caspase-8 activation in apoptosis-resistant but not apoptosis-sensitive colon cancer cells. In a mouse model of inflammation-associated colon tumors, we found nuclear expression of β-catenin, resistance to TNF-induced apoptosis, and reactivation of apoptosis in vivo after cotreatment of TNF with a V-ATPase inhibitor. Together these results suggest that activated β-catenin can facilitate endosomal trafficking of internalized TNF to suppress caspase-8 activation in colon cancer cells.

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