Vitamin A inhibits ornithine decarboxylase (ODC) induction in G1 phase of the cell cycle of synchronous cultures of Chinese hamster ovary (CHO) cells. The retinol-promoted inhibition of ODC was not the result of an effect on general protein synthesis, was effective only in G1 prior to the time an increase in ODC activity had begun, did not involve disruption of the G1-phase increase in cyclic adenosine 3′:5′-monophosphate-dependent protein kinase activity, and required transcription-dependent events for reversal. The inhibition of ODC induction was associated with a block of cell cycle progression in G1 phase. In the presence of the vitamin, there was no incorporation of [3H]thymidine, no induction of S-phase-dependent S-adenosyl-l-methionine decarboxylase, and no ultimate cell doubling. The inhibition of ODC and the inhibition of S-phase transition displayed a similar concentration dependence, with 60% inhibition occurring in the presence of 80 µm retinol, a similar dependence on cell locus in early G1 phase for efficacy, and a similar reversal after removal of the vitamin, with the increase in ODC preceding the increase in S-phase transition in a parallel fashion. Arrest of the cells at the G1 retinol-sensitive restriction point prior to ODC induction resulted in the inhibition of the G1-phase-dependent increase in RNA synthesis.

Other naturally occurring retinoids also inhibit CHO cell growth (retinal > retinol > retinyl acetate > retinoic acid). Retinal, the most potent, displayed a paradoxical effect on CHO cells. At very low concentrations (1 to 5 µm), retinal stimulated CHO growth parameters; ODC activity was enhanced in a parallel fashion. At higher concentrations, retinal inhibited in a manner similar to that described for retinol.


This work was supported by USPHS Research Grant CA-14783 from the National Cancer Institute.

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