Mechanistic aspects of the delay in the G2 phase of the cell cycle caused by tumor promoter 12-O-tetradecanoylphorbol-13-acetate in HeLa cells
- 1 September 1985
- journal article
- research article
- Published by Oxford University Press (OUP) in Carcinogenesis: Integrative Cancer Research
- Vol. 6 (9), 1375-1378
- https://doi.org/10.1093/carcin/6.9.1375
Abstract
In order to gain an insight into the nature of the radiomimetic activity by which the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) alters cell cycle parameters in HeLa cells, possibilities of modifying the TPA-induced G 2 block and recovery from it were studied. TPA-induced G 2 blockage was analysed by counting mitotic figures. It was not influenced by hydroxyurea (10 −3 M) thus indicating that it is independent of DNA synthesis. TPA-induced decrease of mitotic activity occurred faster than that caused by cycloheximide (10 −5 M) indicating that the TPA-sensitive transition point in G 2 is closer to mitosis than that for cycloheximide. Superoxide dismutase, catalase, α-tocopherol, the radioprotector S-(2-aminoethyl)isothiuroniumbromide.HBr (AET), caffeine and indomethacin and eicosatetraynoic acid (ETYA), both inhibitors of oxygenases in the arachidonic acid cascade, were not capable of reducing the TPA-induced G 2 response. Under certain conditions small concentrations of AET (10 −8 M) and ETYA (10 −8 M) appeared to improve recovery slightly. Mannitol and sorbitol, however, both hydroxyl radical scavengers at 0.1 M concentration reduced TPA-effectiveness to a large degree (0.1 M D- and L-mannose were ineffective). Dimethylsulfoxide (0.1 M), another hydroxyl radical scavenger, was ineffective.Keywords
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