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

Authors
 H.-N. Cho  ;  S.-J. Lee  ;  S.-H. Park  ;  Y. J. Lee  ;  C.-K. Cho  ;  Y.-S. Lee 
Citation
 INTERNATIONAL JOURNAL OF RADIATION BIOLOGY, Vol.77(2) : 225-233, 2001 
Journal Title
 INTERNATIONAL JOURNAL OF RADIATION BIOLOGY 
ISSN
 0955-3002 
Issue Date
2001
MeSH
Animals ; Blotting, Western ; CDC2 Protein Kinase/metabolism ; CDC2-CDC28 Kinases* ; Cell Cycle/radiation effects* ; Cyclin A/metabolism ; Cyclin B/metabolism ; Cyclin B1 ; Cyclin D1/antagonists & inhibitors ; Cyclin E/antagonists & inhibitors ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinases/biosynthesis ; Cyclins/metabolism ; Electrophoresis, Polyacrylamide Gel ; Flow Cytometry ; Heat-Shock Proteins* ; Mice ; Neoplasm Proteins/biosynthesis* ; Phosphotransferases/metabolism ; Precipitin Tests ; Protein-Serine-Threonine Kinases/biosynthesis ; Radiation, Ionizing* ; Time Factors ; Tumor Cells, Cultured
Abstract
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.
Full Text
http://www.tandfonline.com/doi/abs/10.1080/09553000010001024
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Radiation Oncology (방사선종양학교실) > 1. Journal Papers
Yonsei Authors
Lee, Yun Sil(이윤실)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/142836
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