Abdallah Rania Abdallah, Abdou Asmaa Gaber, Abdelwahed Moshira, Ali Hend
Department of Pathology, Faculty of Medicine, Menoufia University, Shebein El Kom, Egypt.
J Microsc Ultrastruct. 2019 Jan-Mar;7(1):19-27. doi: 10.4103/JMAU.JMAU_46_18.
Different theories have been postulated to explain the development of nodular prostatic hyperplasia (NPH). Epithelial to mesenchymal transition (EMT) is a physiologic process in which the epithelial cells lose their polarity and cell-cell adhesion and acquire a mesenchymal phenotype.
The aim of the present study is to investigate the potential role of E- and N-cadherin in the induction of EMT in NPH and prostatic carcinoma.
This study was carried out on 55 cases of NPH and 20 cases prostatic carcinoma for evaluation of immunohistochemical expression of E and N cadherins.
Most NPH (54/55 cases, 98.2%) and all cases of prostatic carcinoma showed positive N-cadherin expression in prostatic glands and stroma. High percentage of N-cadherin expression by stromal cells was significantly in favor of prostatic carcinoma compared to NPH. High percentage of N-cadherin expression by epithelial cells of carcinoma group was significantly associated with young age while its high expression by stromal cells was significantly associated with multicentricity. About 96.4% of NPH and 75% of prostatic carcinoma showed positive E-cadherin expression with a significant difference. No significant association between E-cadherin and N-cadherins in both NPH and prostatic carcinoma was identified.
The prominent expression of N-cadherin in large numbers of NPH and prostate carcinoma cases in the epithelial and stromal components could point to the occurrence of EMT in those diseases. It also opens a new gate for treatment of those patients by targeting N-cadherin molecule. The absence of inverse association between E-cadherin and N-cadherins in NPH and prostatic carcinoma may indicate that cadherin switch is not an essential step for the development of EMT.
已经提出了不同的理论来解释结节性前列腺增生(NPH)的发展。上皮-间质转化(EMT)是一种生理过程,其中上皮细胞失去其极性和细胞间粘附,并获得间质表型。
本研究的目的是探讨E-钙粘蛋白和N-钙粘蛋白在NPH和前列腺癌中诱导EMT的潜在作用。
本研究对55例NPH患者和20例前列腺癌患者进行了研究,以评估E钙粘蛋白和N钙粘蛋白的免疫组化表达。
大多数NPH(54/55例,98.2%)和所有前列腺癌病例在前列腺腺体和基质中均显示N-钙粘蛋白阳性表达。与NPH相比,基质细胞中高比例的N-钙粘蛋白表达明显有利于前列腺癌。癌组织上皮细胞中高比例的N-钙粘蛋白表达与年轻年龄显著相关,而基质细胞中高表达与多中心性显著相关。约96.4%的NPH和75%的前列腺癌显示E-钙粘蛋白阳性表达,差异有统计学意义。在NPH和前列腺癌中,未发现E-钙粘蛋白和N-钙粘蛋白之间存在显著关联。
大量NPH和前列腺癌病例的上皮和基质成分中N-钙粘蛋白的显著表达可能表明这些疾病中发生了EMT。这也为通过靶向N-钙粘蛋白分子治疗这些患者开辟了新的途径。NPH和前列腺癌中E-钙粘蛋白和N-钙粘蛋白之间不存在负相关可能表明钙粘蛋白转换不是EMT发展的必要步骤。