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학술저널
저자정보
Xu, Lu-Wei (Department of Urology, Nanjing First Hospital Affiliated to Nanjing Medical University) Qian, Ming (Department of Urology, Nanjing First Hospital Affiliated to Nanjing Medical University) Jia, Rui-Peng (Department of Urology, Nanjing First Hospital Affiliated to Nanjing Medical University) Xu, Zheng (Department of Urology, Nanjing First Hospital Affiliated to Nanjing Medical University) Wu, Jian-Ping (Department of Urology, Nanjing First Hospital Affiliated to Nanjing Medical University) Li, Wen-Cheng (Department of Urology, Nanjing First Hospital Affiliated to Nanjing Medical University) Huang, Wen-Bin (Department of Pathology, Nanjing First Hospital Affiliated to Nanjing Medical University) Chen, Xing-Guo (Center of Lab, Nanjing First Hospital Affiliated to Nanjing Medical University)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제13권 제4호
발행연도
2012.1
수록면
1,639 - 1,644 (6page)

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The aim of this study was to investigate the expression and significance of microsomal prostaglandin synthase-1 (mPGES-1) and Beclin-1 in the development of prostate cancer (PCa). Immunohistochemistry was performed on paraffin-embedded sections with rabbit polyclonal against mPGES-1 and Beclin-1 in 40 PCa, 40 benign prostatic hyperplasia (BPH) and 10 normal prostate specimens for this purpose. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied for mRNA expression of mPGES-1 and Beclin-1, while MTT assays were used to ascertain the best working concentration of the mPGES-1 inhibitor (CAY10526). The effect of CAY10526 treatment on expression of Beclin-1 in DU-145 cells was studied using Western blot analysis. Localization of Beclin-1 and mPGES-1 was in endochylema. Significant differences in expression was noted among PCa, BPH and normal issues (P<0.05). Beclin-1 expression inversely correlated with mPGES-1 expression in PCa tissue (P<0.05). CAY10526 could significantly block mPGES-1 expression and the proliferation of DU-145 cells (P<0.05), while increasing Beclin-1 levels (P<0.05). Overexpression of mPGES-1 could decrease the autophagic PCa cell death. Inhibiting the expression of mPGES-1 may lead to DU-145 cell death and up-regulation of Beclin-1. The results suggest that inhibition of mPGES-1 may have therapeutic potential for PCa in the future.

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