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© 1985 Oxford University Press

research-article

Normal and transformed human prokeratinocytes express divergent effects of a tumor promoter on cell cycle-mediated control of proliferation and differentiation

John J. Wille, Jr. 1, Mark R. Pittelkow 2 and Robert E. Scott 1 3

1Department of Pathology and Cell Biology, Mayo Clinic/Foundation Rochester, MN 55905, USA
2Department of Dermatology, Mayo Clinic/Foundation Rochester, MN 55905, USA

3To whom reprint requests should be sent: 511B Guggenheim Building, Mayo Clinic, Rochester, MN 55905, USA

The tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), is shown to be a potent inhibitor of growth of normal human prokeratinocytes (HPK) cultured in serum-free medium. More specifically TPA inhibits the clonal growth of low density HPK cultures in a dose-dependent manner and the anti-proliferative effect of TPA is selective in that the inactive phorbol diester, 4-{alpha}-12, 13-phorbol didecanoate, does not exert a similar effect. One-hour pulse exposure of HPK to TPA also has an effect comparable with continuous exposure to TPA; both treatments induce rapid growth arrest. Flow cytofluorometric analysis of DNA content shows that in TPA-treated HPK growth arrest is associated with accumulation of cells in both the G1 and G2/M phases of the cell cycle. Most interestingly, the data establish that the growth arrest of HPK induced by TPA is irreversible in that treated cells lose their colony-forming potential and that such cells are committed to differentiate without further cell cycle progression when placed in differentiation-promoting medium. In contrast, a human squamous carcinoma cell line, designated SCC-25, is insensitive to the anti-proliferative effect of TPA regardless of whether these cells are cultured in either serum-containing or serum-free medium. These data are interpreted to suggest that transformed human epithelial cells SCC-25 are defective in their ability to regulate their proliferation and differentiation by TPA-sensitive cell cycle-dependent mechanisms.


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