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Effects of the Bowman‐Birk inhibitor on growth, invasion, and clonogenic survival of human prostate epithelial cells and prostate cancer cells *
Author(s) -
Kennedy Ann R.,
Wan X. Steven
Publication year - 2002
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.10041
Subject(s) - lncap , clonogenic assay , du145 , prostate cancer , matrigel , prostate , biology , gentamicin protection assay , cancer research , cell , cancer , medicine , metastasis , angiogenesis , biochemistry
BACKGROUND The Bowman‐Birk inhibitor (BBI) is a soybean‐derived serine protease inhibitor with demonstrated anticarcinogenic activity in both in vitro and in vivo systems. METHODS The effects of BBI and BBI Concentrate (BBIC), a soybean concentrate enriched in BBI, on cell growth, invasion, and/or survival were evaluated by the sulforhodamine B assay, a colony formation assay, the trypan blue dye exclusion assay and an in vitro invasion assay. The cells used in these studies were normal human prostate epithelial cells and prostate epithelial cell lines derived from embryonic prostate tissue (267B1) or benign prostatic hyperplasia (BPH) tissue (BRF‐55T) and human prostate cancer cells established by Ki‐ras oncogene transfection of 267B1 cells (267B1/Ki‐ras) or from metastatic lesions of human prostate cancer (LNCaP and PC‐3). RESULTS BBIC had a statistically significant inhibitory effect on the growth and clonogenic survival of BRF‐55T, 267B1/Ki‐ras, LNCaP, and PC‐3 cells. BBI also inhibited the growth of LNCaP cells and the clonogenic survival of BRF‐55T and 267B1/Ki‐ras cells and decreased the ability of LNCaP cells to invade across reconstituted basement membrane (Matrigel) when PC‐3 cell‐conditioned medium was utilized as the chemoattractant. BBI or BBIC did not affect the growth of normal prostate epithelial cells. CONCLUSION BBI and/or BBIC could be a useful agent for treatment of prostate diseases. Prostate 50: 125–133, 2002. © 2002 Wiley‐Liss, Inc.