Please use this identifier to cite or link to this item:
Title: Prevention of tumor necrosis factor (TNF)-mediated induction of p21 (WAF1/CIP1) sensitizes MCF-7 carcinoma cells to TNF-induced apoptosis
Authors: Jiang, Y. 
Porter, A.G. 
Keywords: Apoptosis
Growth regulation
p21 induction
Issue Date: 28-Apr-1998
Citation: Jiang, Y., Porter, A.G. (1998-04-28). Prevention of tumor necrosis factor (TNF)-mediated induction of p21 (WAF1/CIP1) sensitizes MCF-7 carcinoma cells to TNF-induced apoptosis. Biochemical and Biophysical Research Communications 245 (3) : 691-697. ScholarBank@NUS Repository.
Abstract: The MCF-7 breast carcinoma and MRC-5 lung fibroblast cell lines are sensitive and resistant to tumor necrosis factor (TNF)-induced apoptosis, respectively. As the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) (p21) is involved in cell cycle regulation and has been implicated in apoptosis, we studied the influence of p21 on growth of MRC-5 cells and on growth and apoptosis in MCF-7 cells. TNF induced p21 mRNA and protein in both cell types, p21 induction by > 0.5 ng/ml TNF in MRC-5 and MCF-7 cells correlated with the inhibition of cell growth. In contrast, < 0.1 ng/ml TNF stimulated MRC-5 (but not MCF-7) cell growth without reduction in p21 levels. TNF-induced apoptosis in MCF-7 cells was first detected after the TNF-mediated increase in p21 and growth arrest had occurred. MCF-7 cells stably transfected with antisense p21 cDNA became more sensitive to TNF-induced apoptosis. Thus, TNF-induced p21 accompanied by growth arrest may counteract or delay TNF cytotoxicity in MCF-7 cells.
Source Title: Biochemical and Biophysical Research Communications
ISSN: 0006291X
DOI: 10.1006/bbrc.1998.8390
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.


checked on Feb 1, 2023


checked on Feb 1, 2023

Page view(s)

checked on Feb 2, 2023

Google ScholarTM



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.