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Carcinogenesis |
B Subunits Induce Epithelial Cell Growth Arrest1
VA Palo Alto Health Care System and the Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305
Nuclear factor 
B (NF-B) gene-regulatory proteins play important
roles in inflammation, neoplasia, and programmed cell death. Recently,
blockade of NF-B function has been shown to result in epithelial
hyperplasia, suggesting a potential role for NF-B in negative growth
regulation. We expressed active NF-B subunits in normal epithelial
cells and found that NF-B profoundly inhibits cell cycle
progression. This growth inhibition is resistant to mitogenic stimuli
and is accompanied by other features of irreversible growth arrest.
NF-B-triggered cell cycle arrest is also associated with selective
induction of the cyclin-dependent kinase inhibitor p21Cip1,
with overexpression of p21Cip1 alone inducing findings
similar to those seen with NF-B in vitro. An active
NF-B subunit expressed in the epidermis of p21Cip1-/-
mice, however, displays only partial growth-inhibitory effects,
suggesting that full NF-B growth inhibition is only partially
p21Cip1 dependent in this setting. These data indicate that
NF-B can trigger cell cycle arrest in epithelial cells in
association with selective induction of a cell cycle inhibitor.
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