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Boric acid induces ER stress and UPR in human prostate DU‐145 and LNCaP cancer cells
Author(s) -
Henderson Kimberly A,
Eckhert Curtis D
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a560
Subject(s) - lncap , prostate cancer , cancer research , prostate , boric acid , cancer , medicine , oncology , chemistry , organic chemistry
The risk of human prostate cancer (PC) is reduced in a dose dependent manner by dietary boron (Oncology Reports, 2004). The proliferation of DU‐145 and LNCaP human PC cells to boric acid is also decreased in a dose dependent manner (Cancer Letters, 2005). Our objective in this study was to establish cellular morphological and proteomic responses to BA. Methods: Cells were exposed to [0, 250 or 1000 μM] BA for 24 h or 6 days and then evaluated for proteomic changes using 2D‐PAGE electrophoresis followed by antibody staining, or morphological changes using transmission and scanning electron microscopy. Results: Expression of calreticulin, Bip/GRP78 and phosphorylated eif2, the hallmarks of the unfolding protein response [UPR], were all increased at 24 h in a dose dependent manner. Six day treatments of PC cells to BA caused dose dependent ER expansion and cellular spreading. Conclusion: These results show that both androgen dependent [LNCaP] and independent [DU‐145] PC cells respond to BA by inducing the UPR. The results identify UPR as a downstream effect of BA‘s inhibition of [Ca]i release [EB 2003] and explain in part, its ability to inhibit cellular proliferation without inducing cell death. Supported by grants DAMD17‐03‐0067 and UC TRSTP.