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Phorbol Ester-induced G₂ Delay in HeLa Cells Analyzed by Time Lapse Photography¹

Institute of Experimental Pathology, German Cancer Research Center, Im Neuenheimer Feld 280, D-6900 Heidelberg, FRG

The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) has been shown previously to mimic X-irradiation in altering cell cycle parameters in Hela cells [Kinzel, V., Richards, J., and Stöhr, M., Science (Wash. DC), 210: 429–431, 1980]. These changes include a delay in G₂ phase from which cells recover in the presence of TPA, which suggests an involvement of cellular mediators. In order to obtain information on the onset and the duration of the G₂ delay, as well as the onset and rate of recovery, a time-lapse study has been carried out. The analysis of cells in prophase shows that at 10^-6 M and 10^-7 M concentrations, TPA and 12-O-retinoylphorbol-13-acetate (RPA) cause a G₂ delay which lasts on the order of 3.5 to 4 h. Below 10^-7 M of RPA and below 10^-8 M of TPA a clear-cut inhibition of HeLa cells in G₂ is no longer detectable by this method. These results for a given phorbol ester are dose dependent within a certain range but unlike the case of X-rays are not proportional to dose. Within the dose range studied the recovery rate follows the opposite order. At 10^-6 M TPA and RPA an indication of a parasynchronous burst is observed. At smaller concentrations or with less biological activity of phorbol ester, the cell multiplication rate approaches that of the control or remains even smaller. Possible reasons are discussed. The determination of the transition points seems to indicate that the cellular events inhibited in G₂ occur shortly before visible prophase.

¹ This work was supported by the Deutsche Forschungsgemeinschaft.

² To whom requests for reprints should be addressed, at Institute of Experimental Pathology, German Cancer Research Center, Im Neuenheimer Feld 280, D-6900 Heidelberg, FRG.

Received 4/10/87. Revised 8/27/87. Revised 11/18/87. Accepted 12/16/87.

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