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Overexpression of heat-shock protein 25 augments radiation-induced cell-cycle arrest in murine L929 cells

 H.-N. Cho  ;  S.-J. Lee  ;  S.-H. Park  ;  Y. J. Lee  ;  C.-K. Cho  ;  Y.-S. Lee 
 International Journal of Radiation Biology, Vol.77(2) : 225-233, 2001 
Journal Title
 International Journal of Radiation Biology 
Issue Date
PURPOSE: Protective effect of small heat-shock protein (sHSP) against gamma-radiation, which associated with HSP25-induced cell-cycle delay and Bcl-2 induction. We further extended our studies on the possible role of HSP25 on ionizing radiation-induced cell-cycle regulation. MATERIALS AND METHODS: Flow-cytometric analyses were performed for cell-cycle distribution and Western blotting. Kinase or immunocomplex kinase assay were performed for detection of cell-cycle protein expression or activation. RESULTS: Pronounced arrest of G1, S and G2/M phase was observed by 4Gy radiation and these arrests were augmented by hsp25 overexpression. Inhibition of cyclin-D1, and cyclin-E and induction of p21Waf by radiation, which was more pronounced in hsp25 overexpressed cells than control cells, which is associated with increased binding activity of CDK2. S-phase regulator, cyclin-A and its associated CDK2 and CDC2 kinase activities were also increased by irradiation and hsp25 overexpression attenuated these phenomena. In addition, cyclin-B1 expression and its associated kinase activity, which are responsible for the transition of G2 to M phase, were increased by radiation and hsp25 overexpression also decreased these phenomena. CONCLUSION: HSP25 augmented radiation-induced cell-cycle arrest (G1, S, and G2/M phase) may be caused by the HSP25-mediated cell-growth delay and is associated with radioresistance.
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1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Radiation Oncology (방사선종양학교실)
Yonsei Authors
이윤실(Lee, Yun Sil)
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