E-, N- and P-cadherin, and alpha-, beta- and gamma-catenin protein expression in normal, hyperplastic and carcinomatous human prostate.
E-, N- and P-cadherin, and alpha-, beta- and gamma-catenin protein expression in normal, hyperplastic and carcinomatous human prostate.
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正常、增生和癌性人类前列腺中 E-、N- 和 P-钙粘蛋白以及 α-、β- 和 γ- 连环蛋白的表达。
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发表时间：
2000
期刊：
影响因子：
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通讯作者：
R. Paniagua
中科院分区：
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作者：
M. Arenas;E. Romo;M. Royuela;B. Fraile;R. Paniagua
采用免疫组化、ELISA、Western blot等方法研究正常前列腺、良性前列腺增生和前列腺癌男性前列腺中E-、N-和P-cadherin、α -、β -和γ -catenin、肌动蛋白的表达，探讨其在这些疾病的发病机制中的可能作用。目前的研究结果表明，增生性前列腺的免疫表型与正常前列腺和癌前列腺在细胞内分布（免疫组化观察）和对钙粘蛋白、连环蛋白和肌动蛋白的免疫反应强度（ELISA测定）上存在差异。与正常前列腺不同，增生性前列腺对三种钙粘蛋白、两种连环蛋白和肌动蛋白的免疫反应较弱，p -钙粘蛋白、β -和γ -连环蛋白和肌动蛋白在细胞内的分布也较弱。良性前列腺增生和前列腺癌之间的差异不太明显，因为增生性前列腺与癌性前列腺的不同之处在于对P-cadherin和α -catenin的免疫反应较弱。本研究最显著的发现是：(1)前列腺癌组织中α -连环蛋白的产生明显高于良性前列腺增生和正常前列腺组织；(2) P-cadherin在良性前列腺增生中的表达较正常前列腺和癌前列腺的表达降低。可以得出结论，对钙粘蛋白、连环蛋白和肌动蛋白的免疫反应降低，以及前列腺细胞中肌动蛋白细胞内分布的变化，并不一定提示恶性肿瘤，因为这些改变也存在于BPH中，因此，钙粘蛋白-连环蛋白介导的粘连丧失本身不足以建立侵袭性表型。
The expression of E-, N- and P-cadherin, alpha-, beta- and gamma-catenin, and actin was studied by immunohistochemistry, ELISA, and Western blot analysis in normal prostates, and in the prostates of men with benign prostatic hyperplasia and men with prostatic carcinoma, in order to evaluate their possible role in the pathogenesis of these diseases. Present results reveal that the immunophenotype of hyperplastic prostates differs from those of both normal and carcinomatous prostates in the intracellular distribution (observed by immunohistochemistry) and the intensity (measured by ELISA) of immunoreactions to cadherins, catenins, and actin. Hyperplastic prostates differ form normal prostates in the weaker immunoreaction to the three cadherin types, the two catenins, and actin, as well as in the intracellular distribution of P-cadherin, beta- and gamma-catenin, and actin. Differences between benign prostatic hyperplasia and prostatic carcinoma are less marked because hyperplastic prostates differ from carcinomatous prostates only in the weaker immunoreactions to P-cadherin, and alpha-catenin. The most remarkable findings in this study were: (1) alpha-catenin production was elevated in prostatic carcinoma in comparison with benign prostatic hyperplasia and normal prostate; and (2) P-cadherin expression in benign prostatic hyperplasia is reduced with regard to those of normal and carcinomatous prostates. It may be concluded that a decreased immunoreaction to cadherins, catenins, and actin, as well as changes in the intracellular distribution of actin in prostatic cells are not necessarily suggestive of malignancy, because these alterations are also present in BPH, and thus, the loss of cadherin-catenin-mediated adhesion alone is not sufficient to establish an invasive phenotype.