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Korean J Urol. 2011 Apr;52(4):253-9. doi: 10.4111/kju.2011.52.4.253. Epub 2011 Apr 22.

Cyclooxygenase-2 overexpression in chronic inflammation associated with benign prostatic hyperplasia: is it related to apoptosis and angiogenesis of prostate cancer?

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  • 1Department of Urology, Keimyung University School of Medicine, Daegu, Korea.



This study was performed to investigate the relationship between cyclooxygenase-2 (COX-2) expression and apoptosis/angiogenesis in inflammatory and noninflammatory benign prostatic hyperplasia (BPH) and prostate cancer (PC).


This study involved 64 BPH and 57 PC patients. The BPH histopathologies were classified by the presence of chronic inflammation as follows: noninflammatory BPH (NI-BPH; n=23) and inflammatory BPH (I-BPH; n=41). The association between the expression of COX-2, expression of Bcl-2, the apoptotic index (AI), expression of vascular endothelial growth factor (VEGF), and microvascular density (MVD) in the prostate was investigated.


An overexpression of COX-2, Bcl-2, and VEGF was observed in cases of PC compared with cases of BPH. In PC, the AI was lower and MVD was higher than in BPH. In NI-BPH, I-BPH, and PC, the overexpression of COX-2, Bcl-2, and VEGF gradually increased. The AI was high in I-BPH, but did not differ significantly between the NI-BPH and I-BPH groups or between the NI-BPH and PC groups. MVD was significantly high in PC, but no significant difference was found between NI-BPH and I-BPH. A significant correlation was shown between the overexpression of COX-2 and Bcl-2, and COX-2 and VEGF. However, the AI was not correlated with the overexpression of COX-2 or Bcl-2. MVD was correlated with the overexpression of COX-2 and VEGF.


COX-2 overexpression in PC is correlated with a decrease in apoptosis and an increase in angiogenesis. Chronic inflammation in BPH causes an overexpression of COX-2, which induces the increased expression of Bcl-2 and VEGF. It is likely that chronic inflammation plays a role in the intermediate step of carcinogenesis in the prostate.


Angiogenesis-inducing agents; Apoptosis; Cyclooxygenase 2; Prostatic hyperplasia; Prostatic neoplasms

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