No abstract

Recent reports have shown that peroxisome proliferatoractivated receptor (PPAR

SummaryWe have recently reported a novel function for carbonyl reductase (CR), namely, its ability to modulate the metastatic potential of malignant mouse cells. Because there are currently no data addressing a similar function for CR in human cancers, the aim of this study was to assess a correlation between survival and metastasis, and CR level in epithelial ovarian cancer. Using anti-CR antibody, immunohistochemical staining was performed on 73 epithelial ovarian cancers, 13 borderline malignant tumours, and 25 benign ovarian tumours for a total of 111 specimens. The combined rate for strongly and weakly positive reactions for CR was 32.0% for benign tumours, 38.5% for borderline malignant tumours, and 61.6% for ovarian cancers. The CR-positive rate was 35.7% (weakly positive alone) for ovarian cancers with retroperitoneal lymph node (RLN) metastasis and 67.8% for those without RLN metastasis (P < 0.05). The 5-year survival rate was 62.7% for the patients with CR-negative cancer and 86.1% for those with CR-positive cancer (P < 0.05). The present results indicate that decreased CR expression in epithelial ovarian cancer is associated with RLN metastasis and poor survival.

No abstract

Expression of cyclooxygenase (COX)-2 plays a key role in tumorigenesis and development and peroxisome proliferator-activated receptor g (PPARg) has been implicated in the control of COX-2 expression in some tissues. The aim of this study is to investigate (1) whether expression of COX-2 and PPARg is associated with ovarian carcinogenesis and progression of ovarian tumours and (2) whether COX-2 expression is controlled through ligand-mediated activation of PPARg in ovarian carcinoma cells. For this purpose, the presence of COX-2 and PPARg was immunohistochemically examined in 71 epithelial ovarian carcinomas, 18 borderline tumours and 23 benign tumours and the levels of COX-2 and PPARg proteins were determined by enzyme immunoassay in four benign tumours, three borderline tumours and 12 carcinomas. The frequency of COX-2 and PPARg detection was significantly increased and decreased as lesions progressed to carcinoma, respectively. The COX-2 protein was not detected in the three borderline tumours, whereas PPARg protein was detected in all of them. COX-2 protein was detected in eight of the 12 carcinomas, whereas PPARg protein was detected in only two cases. In addition, PPARg protein was not detected in all of the eight carcinomas in which COX-2 protein was detected, suggesting that expression of PPARg and COX-2 was in a reciprocal relationship. Furthermore, in cultured ovarian carcinoma cells, Western blot revealed that PPARg and COX-2 expression was regulated conversely as a result of stimulation by 15-deoxy-D 12, 14 PGJ 2 (15-PGJ 2 ), a PPARg activator. In addition, 15d-PGJ 2 suppressed tumour necrosis factor-ainduced-COX-2 expression, confirming the reciprocal correlation between COX-2 and PPARg. From these results, it was suggested that PPARg activation might suppress COX-2 expression via the nuclear factor-kB pathway in the ovarian carcinoma cells and that low expression of PPARg and high expression of COX-2 might be involved in carcinogenesis and progression of ovarian tumours.