Premium
Effect of ultraviolet (UV) A, UVB or ionizing radiation on the cell cycle of human melanoma cells
Author(s) -
Placzek M.,
Przybilla B.,
Kerkmann U.,
Gaube S.,
Gilbertz K.P.
Publication year - 2007
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2007.07795.x
Subject(s) - cell cycle , pyrimidine dimer , mitosis , flow cytometry , dna damage , melanoma , cell , ionizing radiation , dna repair , cell cycle checkpoint , bromodeoxyuridine , chemistry , irradiation , microbiology and biotechnology , dna , biology , cancer research , cell growth , biochemistry , physics , nuclear physics
Summary Background One important component of the cellular response to irradiation is the activation of cell cycle checkpoints. It is known that both ultraviolet (UV) radiation and ionizing radiation (IR) can activate checkpoints at transitions from G 1 to S phase, from G 2 phase to mitosis and during DNA replication. Objectives To evaluate the effects of irradiation with different wavelengths on cell cycle alterations. Methods p53‐deficient IPC‐298 melanoma cells were irradiated with 10 J cm −2 UVA, 40 mJ cm −2 UVB, or with 7·5 Gy IR. Cell cycle effects were then determined by DNA/5‐bromodeoxyuridine dual‐parameter flow cytometry. Results IPC‐298 cells irradiated in G 1 with UVA were not arrested at the G 1 /S transition, but at the G 2 /M transition. Despite p53 deficiency, the cells showed a G 1 arrest after UVB exposure. Furthermore, IR did not affect G 1 or S phase, but induced G 2 phase arrest. Hence, the effects of UVA, but not of UVB, on the cell cycle in p53‐deficient melanoma cells are comparable with those of IR. Conclusions UVA and IR induce radical‐mediated strand breaks and DNA lesions, and UVB essentially induces thymine dimers that lead to excision repair‐related strand breaks. Different cell cycle effects may be a consequence of different types of DNA damage. The results showed that UVB‐irradiated p53‐deficient cells are arrested in G 1 . Irradiation with the solar radiation component UVB can therefore result in a beneficial retardation of tumour promotion in human skin carrying p53‐mutated cell clones.