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Effect of ionizing radiation on cell‐cycle progression and cyclin B 1 expression in human melanoma cells
Author(s) -
Villa Raffaella,
Zaffaroni Nadia,
Bearzatto Alessandra,
Costa Aurora,
Sichirollo Adele,
Silvestrini Rosella
Publication year - 1996
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19960328)66:1<104::aid-ijc18>3.0.co;2-d
Subject(s) - ionizing radiation , cancer research , melanoma , cyclin , cell cycle , cell cycle progression , cyclin d , medicine , biology , cell , irradiation , genetics , physics , nuclear physics
In the present study we investigated the effect of γ‐irradiation (2.5 and 10 Gy) on cell‐cycle progression of a human melanoma cell line, M14, characterized by a moderate radiosensitivity (SF2 = 0.5). Flow cytometric analysis showed a dose‐dependent S‐phase accumulation, which was detectable 8 hr after treatment with 2 and 5 Gy and was still persistent at 12 hr after 10 Gy exposure. Such a delay in S‐phase was paralleled or followed by an accumulation of cells in G 2 M, which was transient at the lowest radiation doses and still persistent at 72 hr after 10 Gy. Such an accumulation was, at least in part, due to a block in G 2 ‐M transition, as demonstrated by mitotic index analysis. Bivariate flow cytometric analysis of DNA content and cyclin B 1 expression showed that, following 2 and 5 Gy, the fraction of cyclin B 1 ‐expressing cells was superimposable upon that of G 2 M cells. Conversely, in cells treated with 10 Gy, the fraction of cyclin B 1 ‐expressing cells was half the G 2 M cell fraction. Northern‐blot analysis indicated that the radiation‐induced decrease in cyclin B 1 protein expression was accompanied by a reduced cyclin B mRNA level. On the whole, our results indicate a direct inhibitory effect of 10 Gy irradiation on cyclin B 1 expression as a possible cause for the persistent G 2 block in irradiated M14 cells. © 1996 Wiley‐Liss, Inc.