Relationship between prostaglandin E2 receptors and clinicopathologic features in human prostate cancer tissue

Relationship between prostaglandin E2 receptors and clinicopathologic features in human prostate cancer tissue
复制标题

DOI:
10.1016/j.urology.2006.09.035
复制
发表时间:
2006-12-01
期刊:
影响因子:
2.1
通讯作者:
Kanetake, Hiroshi
Kanetake, Hiroshi
中科院分区:
医学4区
文献类型:
--
作者:
Miyata, Yasuyoshi;Kanda, Shigeru;Kanetake, Hiroshi

文献摘要

被引文献

相似文献

目标.前列腺素E-2参与致癌过程和恶性侵袭性。这些作用是通过与四种特定的E型前列腺素(EP)受体(EP 1 R至EP 4 R)结合来介导的。尽管EPR在多种癌症中过表达,但其表达模式在不同癌症类型中不同。本研究的目的是阐明前列腺癌中EPR的临床意义。我们用免疫组化方法检测了122例前列腺癌组织中EPR的表达。我们还研究了EPR与癌细胞增殖的关系。癌细胞中EP 1 R的免疫阳性率(36.3% +/- 14.3%)显著高于(P < 0.01)(7.1% +/- 4.8%),与Gleason评分呈正相关T分期(P < 0.01)、N分期(P = 0.03)、M分期(P < 0.01)与癌细胞增殖相关(r = 0.35,P < 0.01)。EP 2 R在癌细胞中的表达(38.9% ± 11.6%)显著高于非癌腺体(30.6% ± 8.6%)(P < 0.01),且与癌细胞增殖有关(P < 0.01)。EP 4 R在癌细胞中的表达也显著高于非癌腺体(P < 0.01)。EP 2 R和EP 4 R的表达与临床病理特征无关,EP 3R的表达与临床病理参数无关。我们的研究结果表明,EP 1 R,EP 2 R和EP 4 R与前列腺癌的发生有关。特别是,EP 1 R似乎在前列腺癌患者的恶性侵袭性和肿瘤发展中起重要作用。
Objectives. Prostaglandin E-2 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.