Cyclooxygenase-2 Overexpression in Chronic Inflammation Associated with Benign Prostatic Hyperplasia: Is It Related to Apoptosis and Angiogenesis of Prostate Cancer?.
10.4111/kju.2011.52.4.253
- Author:
Byung Hoon KIM
1
;
Chun Il KIM
;
Hyuk Soo CHANG
;
Mi Sun CHOE
;
Hye Ra JUNG
;
Duk Yoon KIM
;
Choal Hee PARK
Author Information
1. Department of Urology, Keimyung University School of Medicine, Daegu, Korea. chp@dsmc.or.kr
- Publication Type:Original Article
- Keywords:
Angiogenesis-inducing agents;
Apoptosis;
Cyclooxygenase 2;
Prostatic hyperplasia;
Prostatic neoplasms
- MeSH:
Apoptosis;
Cyclooxygenase 2;
Humans;
Inflammation;
Prostate;
Prostatic Hyperplasia;
Prostatic Neoplasms;
Vascular Endothelial Growth Factor A
- From:Korean Journal of Urology
2011;52(4):253-259
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: 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). MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
