Effect of ultraviolet (UV) A, UVB or ionizing radiation on the cell cycle of human melanoma cells

• Published in: British journal of dermatology (1951) Vol. 156; no. 5; pp. 843 - 847
• Main Authors: Placzek, M., Przybilla, B., Kerkmann, U., Gaube, S., Gilbertz, K.-P.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01-05-2007; Blackwell
• Subjects: Biological and medical sciences; cell cycle; Cell Cycle - radiation effects; Dermatology; DNA Damage; Humans; ionizing radiation; Medical sciences; melanoma; Melanoma - pathology; Pyrimidine Dimers; Radiation, Ionizing; Skin Neoplasms - pathology; Tumors of the skin and soft tissue. Premalignant lesions; ultraviolet radiation; Ultraviolet Rays - adverse effects; Human; Cell culture; UVA radiation; Dermatology; UVB radiation; melanoma; Malignant tumor; sltroviolet radiation; Ultraviolet radiation; Ionizing radiation; Cell cycle; Malignant melanoma; Tumor cell
• DOI: 10.1111/j.1365-2133.2007.07795.x
• EISSN: 1365-2133
• ISSN: 0007-0963

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 G1 to S phase, from G2 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 G1 with UVA were not arrested at the G1/S transition, but at the G2/M transition. Despite p53 deficiency, the cells showed a G1 arrest after UVB exposure. Furthermore, IR did not affect G1 or S phase, but induced G2 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 G1. 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.