14-3-3.sigma. arrests the cell cycle

C - Chemistry – Metallurgy – 12 – N

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C12N 15/12 (2006.01) A61K 38/17 (2006.01) A61K 48/00 (2006.01) C07K 14/47 (2006.01) C12N 5/08 (2006.01) C12N 5/10 (2006.01) C12N 15/11 (2006.01) C12N 15/85 (2006.01) G01N 33/50 (2006.01) A61K 38/00 (2006.01)

Patent

CA 2315279

Exposure of colorectal cancer (CRC) cells to ionizing radiation results in a growth arrest, with cells blocked in both the G1 and G2 phases of the cell cycle. The G1 block has been shown to be due to the p53-mediated induction of the cyclin-dependent kinase inhibitor p21WAF1/CIP1/SDI1, but the basis for the G2 arrest is unknown. Through a quantitative analysis of gene expression patterns in CRC cell lines, we have discovered that 14-3-3.sigma. is strongly induced by .gamma.-irradiation and other DNA-damaging agents. The induction of 14-3-3.sigma. is mediated by a p53-responsive element located 1.815 kb upstream of its transcription start site. Exogenous introduction of 14-3- 3.sigma. into cycling cells results in a G2 block similar to that observed following irradiation. These results document a molecular mechanism for G2/M control that is regulated in human cells by p53.

L'exposition d'un cancer colorectal (CRC) à un rayonnement ionisant entraîne un arrêt de la croissance, les cellules restant bloquées dans les phases G1 et G2 du cycle cellulaire. Il a été démontré que le blocage en G1 résulte de l'induction à médiation p53 de l'inhibiteur p21?WAF1/CIP1/SDI1¿ de kinase dépendant de la cycline, mais on ne connaît pas la cause du blocage en G2. A l'aide d'une analyse quantitative des motifs d'expression génique dans les lignées cellulaires du CRC, nous avons découvert que 14-3-3.sigma. est fortement induit par le rayonnement .gamma. et d'autres agents endommageant l'ADN. L'induction de 14-3-3.sigma. se produit sous la médiation d'un élément sensible à p-53 situé à 1,815 kb en amont de son site de début de transcription. L'introduction exogène de 14-3-3.sigma. dans les cellules proliférantes provoque un blocage en G2 similaire à celui qui est observé à la suite d'une irradiation. Ces résultats démontrent un mécanisme moléculaire de blocage G2/M qui, dans les cellules humaines, est régulé par p53.

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