Complete Elimination of Colorectal Tumor Xenograft by Combined Manganese Superoxide Dismutase with Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand Gene Virotherapy

2006 ◽  
Vol 66 (8) ◽  
pp. 4291-4298 ◽  
Author(s):  
Yanhong Zhang ◽  
Jinfa Gu ◽  
Lili Zhao ◽  
Lingfeng He ◽  
Wenbin Qian ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Manganese Superoxide Dismutase ◽  
Colorectal Tumor ◽  
Tumor Xenograft ◽  
Complete Elimination ◽  
Manganese Superoxide ◽  
Necrosis Factor

The effect of tumor necrosis factor-α on human malignant glial cells

1992 ◽  
Vol 76 (4) ◽  
pp. 652-659 ◽  
Author(s):  
Rolando F. Del Maestro ◽  
Monica Lopez-Torres ◽  
Warren B. McDonald ◽  
Eric C. Stroude ◽  
Indrasen S. Vaithilingam
Keyword(s):  
Superoxide Dismutase ◽  
Tumor Necrosis Factor ◽  
Cell Line ◽  
Tumor Necrosis ◽  
Manganese Superoxide Dismutase ◽  
Tumor Necrosis Factor Α ◽  
Superoxide Dismutase Activity ◽  
Manganese Superoxide ◽  
Factor Α ◽  
Necrosis Factor

✓ The influence of human recombinant tumor necrosis factor-α has been assessed on a cell line (U-251) derived from a human malignant glial tumor. The results of this study demonstrate that tumor necrosis factor-α at doses of 50 and 100 ng/ml: 1) did not have cytotoxic or cytostatic effects on the U-251 cell line; 2) significantly increased the intracellular activity of manganese superoxide dismutase but had no effect on copper and zinc superoxide dismutase, catalase, or glutathione peroxidase activity; and 3) did not significantly alter the intracellular or extracellular general protease and collagenase type IV activity of these cells. The resistance of the U-251 cell line to tumor necrosis factor-α cytotoxicity may be related in part to the high intrinsic manganese superoxide dismutase activity present in this cell line combined with the ability of this cell line to induce substantial amounts of protective manganese superoxide dismutase activity in response to tumor necrosis factor-α.

scholarly journals Regulation of manganese superoxide dismutase and other antioxidant genes in normal and leukemic hematopoietic cells and their relationship to cytotoxicity by tumor necrosis factor

Blood ◽  
1993 ◽  
Vol 82 (4) ◽  
pp. 1142-1150 ◽  
Author(s):  
M Kizaki ◽  
A Sakashita ◽  
A Karmakar ◽  
CW Lin ◽  
HP Koeffler
Keyword(s):  
Superoxide Dismutase ◽  
Tumor Necrosis Factor ◽  
Cell Lines ◽  
Tumor Necrosis ◽  
Manganese Superoxide Dismutase ◽  
Hematopoietic Cells ◽  
Antioxidant Genes ◽  
Normal Peripheral Blood ◽  
Manganese Superoxide ◽  
Necrosis Factor

Myeloid cells are a major source of superoxide and other oxygen metabolites. As a protective mechanism, cells express antioxidant enzymes including manganese superoxide dismutase (Mn-SOD), copper-zinc SOD (Cu/Zn-SOD), and glutathione peroxidase (GSX-PX). Even though hematopoietic cells are a major source of oxidants, little is known of their expression of antioxidants. We found that seven myeloid leukemic cell lines blocked at different stages of differentiation constitutively expressed Mn-SOD, Cu/Zn-SOD, and GSX-PX RNAs. Level of Mn-SOD activities paralleled levels of Mn-SOD RNA. Terminal differentiation of native HL-60 cells to either granulocytes or macrophages did not alter levels of Mn-SOD RNA but markedly decreased cell division. Myeloid leukemic lines sensitive to cytotoxic effects of tumor necrosis factor (TNF) as well as normal peripheral blood lymphocytes and monocytes, dramatically increased their levels of Mn- SOD RNA in the presence of TNF. In contrast, Cu/Zn-SOD and GSX-PX RNA levels did not increase in these same cells. TNF-resistant leukemic lines had higher constitutive levels of Mn-SOD RNA and activity; and these levels did not change in the presence of TNF. Antisense but not random oligonucleotides to Mn-SOD markedly increased the sensitivity to the inhibitory effects of TNF for both the native HL-60 (TNF-sensitive) and K562 (TNF-resistant) cell lines. Further studies showed that the antisense oligonucleotides entered the cells and resulted in decreased levels of Mn-SOD RNA. The data suggest that Mn-SOD may provide protection against cytotoxicity of TNF in hematopoietic cells.

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