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© 1988 Oxford University Press

research-article

Effects of palytoxin or ouabain on growth and squamous differentiation of human bronchial epithelial cells in vitro

Claude Bonnard 1, John F. Lechner 2, Brenda I. Gerwin 2, Hirota Fujiki 3 and Curtis C. Harris 2 4

1Nestle Research Center Nestec Ltd, Vers-chez-les-Blanc, CH-1020 Lausanne, Switzerland
2Laboratory of Human Carcinogcnesis Bldg. 37, Rm. 2C01 Division of Cancer Etiology, National Cancer Institute Bethesda, MD 20892, USA
3National Cancer Center Research Institute Tsukiji 5-chrome Chuo-Ku, Tokyo 104, Japan

4To whom correspondence should be addressed

The effects of the non-12-O-tetradecanoylphorbol-13-acetate type tumor promoter palytoxin on human bronchial epithelial cells was studied in an in vitro serum-free culture system. Unlike the results of previous studies with another tumor promoter, 12-O-tetradecanoylphorbol-13-acetate, palytoxin did not induce squamous differentiation of normal bronchial epithelial cells and was equally cytotoxic for normal human bronchial epithelial cells, a human lung tumor cell line, and human bronchial epithelial cells immortalized by infection with adenovirus 12-SV40 hybrid virus (BEAS-2B cells). Palytoxin did not induce a change in free cytosolic Ca2+ concentration of BEAS-2B cells. The effect of palytoxin on the c-myc mRNA steady state level in BEAS-2B cells was studied: 1 pM palytoxin increased the steady-state level at 12 and 18 h. Furthermore, the induction was accompanied by an increase in [3H]thymidine uptake. Because palytoxin binds to (Nat+ + K+ATPase, the effects of ouabain were compared to the effects of palytoxin. A ouabain-resistant cell line was as sensitive to the growth inhibitory effect of palytoxin as the parent ouabain-sensitive cell line, suggesting different binding sites to the (Na+ + K+-ATPase for palytoxin and ouabain. Ouabain also increased the steady-state level of c-myc gene expression, but earlier than palytoxin, and the increase in the level of c-myc mRNA was accompanied by a drop in DNA synthesis. These results suggest that palytoxin does not act by growth stimulation, differential cytotoxicity or terminal differentiation of normal versus neoplastic cells which are proposed mechanisms of tumor promotion.


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 Am. J. Physiol. Cell Physiol.Home page
E. V. Wattenberg
Palytoxin: exploiting a novel skin tumor promoter to explore signal transduction and carcinogenesis
Am J Physiol Cell Physiol, January 1, 2007; 292(1): C24 - C32.
[Abstract] [Full Text] [PDF]


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