OBJECTIVES: Prostaglandin E2 is involved in the carcinogenic process and malignant aggressiveness. These effects are mediated through binding to four specific type E prostanoid (EP) receptors (EP1R to EP4R). Although EPRs are overexpressed in a variety of cancers, their expression pattern varies among different cancer types. The aim of this study was to clarify the clinical significance of EPRs in prostate cancer. METHODS: We examined the expression of each EPR in 122 prostate cancer tissue samples by immunohistochemistry. We also investigated the relationship between EPRs and cancer cell proliferation. RESULTS: The rate of immunopositivity for EP1R in cancer cells (36.3% +/- 14.3%) was significantly greater (P < 0.01) than in nontumor glands (7.1% +/- 4.8%) and correlated positively with the Gleason score (P < 0.01), T stage (P < 0.01), N stage (P = 0.03), M stage (P < 0.01), and cancer cell proliferation (r = 0.35, P < 0.01). The EP2R expression in cancer cells (38.9% +/- 11.6%) was significantly greater (P < 0.01) than in nontumor glands (30.6% +/- 8.6%), and correlated with cancer cell proliferation (P < 0.01). The EP4R expression in cancer cells was also significantly greater (P < 0.01) than in nontumor glands. However, the expression of EP2R and EP4R did not correlate with the clinicopathologic features and EP3R expression was not associated with any parameters. CONCLUSIONS: Our results have indicated that EP1R, EP2R, and EP4R are associated with prostate carcinogenesis. In particular, the EP1R seems to play an important role in malignant aggressiveness and tumor development in patients with prostate cancer.
OBJECTIVES:Prostaglandin E2 is involved in the carcinogenic process and malignant aggressiveness. These effects are mediated through binding to four specific type E prostanoid (EP) receptors (EP1R to EP4R). Although EPRs are overexpressed in a variety of cancers, their expression pattern varies among different cancer types. The aim of this study was to clarify the clinical significance of EPRs in prostate cancer. METHODS: We examined the expression of each EPR in 122 prostate cancer tissue samples by immunohistochemistry. We also investigated the relationship between EPRs and cancer cell proliferation. RESULTS: The rate of immunopositivity for EP1R in cancer cells (36.3% +/- 14.3%) was significantly greater (P < 0.01) than in nontumor glands (7.1% +/- 4.8%) and correlated positively with the Gleason score (P < 0.01), T stage (P < 0.01), N stage (P = 0.03), M stage (P < 0.01), and cancer cell proliferation (r = 0.35, P < 0.01). The EP2R expression in cancer cells (38.9% +/- 11.6%) was significantly greater (P < 0.01) than in nontumor glands (30.6% +/- 8.6%), and correlated with cancer cell proliferation (P < 0.01). The EP4R expression in cancer cells was also significantly greater (P < 0.01) than in nontumor glands. However, the expression of EP2R and EP4R did not correlate with the clinicopathologic features and EP3R expression was not associated with any parameters. CONCLUSIONS: Our results have indicated that EP1R, EP2R, and EP4R are associated with prostate carcinogenesis. In particular, the EP1R seems to play an important role in malignant aggressiveness and tumor development in patients with prostate cancer.
Authors: Agnes Rasmuson; Anna Kock; Ole Martin Fuskevåg; Björn Kruspig; Jaione Simón-Santamaría; Vladimir Gogvadze; John Inge Johnsen; Per Kogner; Baldur Sveinbjörnsson Journal: PLoS One Date: 2012-01-19 Impact factor: 3.240
Authors: Xiaoyong Huang; Samira Taeb; Sahar Jahangiri; Elina Korpela; Ivan Cadonic; Nancy Yu; Sergey N Krylov; Emmanouil Fokas; Paul C Boutros; Stanley K Liu Journal: Oncotarget Date: 2015-09-08