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Proliferation of DU145 prostate cancer cells is inhibited by suppressing insulin-like growth factor binding protein-2

Authors
 SHILLA CHATTERJEE  ;  EUN SUNG PARK  ;  MELVYN S. SOLOFF 
Citation
 INTERNATIONAL JOURNAL OF UROLOGY, Vol.11(10) : 876-884, 2004 
Journal Title
 INTERNATIONAL JOURNAL OF UROLOGY 
ISSN
 0919-8172 
Issue Date
2004
Keywords
IGFBP‐2 suppression ; growth inhibition ; prostate cancer.
Abstract
BACKGROUND: Insulin-like growth factor binding protein-2 (IGFBP-2) is expressed by all human prostate cancer cell lines and dramatically increases in the serum of prostate cancer patients. However, the role of IGFBP-2 in prostatic tumorigenesis is not known. The aim of the present study was to investigate the effects of IGFBP-2 on the proliferation of DU145 human prostate cancer cells in culture. METHODS: Using cell proliferation assays, we examined the effects of exogenously administered and endogenously modulated levels of IGFBP-2 on the proliferation of DU145 cells. RESULT: Cell growth was stimulated by exogenously administered IGFBP-2, but significantly retarded (P < 0.05) by its neutralizing antibody. Overexpression of IGFBP-2 by transfection also stimulated cell growth, which was significantly (P < 0.05) inhibited in transfectants expressing antisense mRNA to IGFBP-2. Furthermore, the proliferation of IGFBP-2 overexpressing cells was significantly dampened by exogenously administered IGFBP-2 antibody. CONCLUSIONS: IGFBP-2 is an autocrine growth factor for DU145 human prostate cancer cells and cell proliferation can be significantly retarded by neutralizing or inhibiting its synthesis. These findings provide a strong rationale for targeting IGFBP-2 in the testing of novel strategies to treat prostate cancer.
Full Text
http://onlinelibrary.wiley.com/doi/10.1111/j.1442-2042.2004.00898.x/abstract
DOI
10.1111/j.1442-2042.2004.00898.x
Appears in Collections:
5. Research Institutes (연구소) > Institute for Medical Convergence (연의-생공연 메디컬융합연구소) > 1. Journal Papers
Yonsei Authors
Park, Eun Sung(박은성)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/111380
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