Tumor necrosis factor-α alters protein metabolism and cell-cycle kinetics in malignant tumor

1996 ◽  
Vol 8 (1) ◽  
pp. 19-22
Author(s):  
Ye Shenglong ◽  
Tang Zhaoyou ◽  
Bruce R Bistrian
2014 ◽  
Vol 62 ◽  
pp. 273-285 ◽  
Author(s):  
Kiran Bhaskar ◽  
Nicole Maphis ◽  
Guixiang Xu ◽  
Nicholas H. Varvel ◽  
Olga N. Kokiko-Cochran ◽  
...  

1996 ◽  
Vol 39 (7) ◽  
pp. 1115-1124 ◽  
Author(s):  
Laura C. Rall ◽  
Clifford J. Rosen ◽  
Gregory Dolnikowski ◽  
Wilburta J. Hartman ◽  
Nancy Lundgren ◽  
...  

1994 ◽  
Vol 34 (5) ◽  
pp. 274-278 ◽  
Author(s):  
Kang CHENG ◽  
Yutaka SAWAMURA ◽  
Shirou SAKUMA ◽  
Mitsuhiro TADA ◽  
Masako SUDO ◽  
...  

1993 ◽  
Vol 265 (2) ◽  
pp. C365-C374 ◽  
Author(s):  
J. M. Wan ◽  
F. Fogt ◽  
B. R. Bistrian ◽  
N. W. Istfan

To determine the significance of protein breakdown in regulating tumor growth and to better understand the antitumor mechanism of tumor necrosis factor in vivo, we measured the effects of a 6-h constant intravenous infusion of human recombinant tumor necrosis factor-alpha (rHuTNF) on tumor protein metabolism and cell cycle kinetics in rats bearing the Walker-256 carcinosarcoma. Protein metabolism was investigated with the use of [14C]leucine infusion; estimates of tumor cell cycle kinetics were obtained in vivo by use of 5-bromo-2'-deoxyuridine (BrdUrd) pulse labeling and bivariate BrdUrd/DNA analysis by flow cytometry. Reduction in tumor growth by rHuTNF was associated with a dose-dependent increase in tumor proteolysis but no change in tumor protein synthesis. At the cellular level, rHuTNF had a significant cytostatic effect on G2/M cells and caused a marked decrease in the fraction of cells capable of BrdUrd uptake. Release of BrdUrd, an indicator of cell death, was noted in only 7.5% of tumor cells labeled at the beginning of rHuTNF infusion. These results suggest that either tumor protein breakdown may influence cell cycle activity by regulating cytoplasmic protein mass or that tumor proteolysis may be a compensatory mechanism for limiting cytoplasmic size when cellular division is interrupted suddenly.


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