Bryan Richard T
School of Cancer Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK
Philos Trans R Soc Lond B Biol Sci. 2015 Feb 5;370(1661):20140042. doi: 10.1098/rstb.2014.0042.
Cadherins are mediators of cell-cell adhesion in epithelial tissues. E-cadherin is a known tumour suppressor and plays a central role in suppressing the invasive phenotype of cancer cells. However, the abnormal expression of N- and P-cadherin ('cadherin switching', CS) has been shown to promote a more invasive and m̀alignant phenotype of cancer, with P-cadherin possibly acting as a key mediator of invasion and metastasis in bladder cancer. Cadherins are also implicated in numerous signalling events related to embryonic development, tissue morphogenesis and homeostasis. It is these wide ranging effects and the serious implications of CS that make the cadherin cell adhesion molecules and their related pathways strong candidate targets for the inhibition of cancer progression, including bladder cancer. This review focuses on CS in the context of bladder cancer and in particular the switch to P-cadherin expression, and discusses other related molecules and phenomena, including EpCAM and the development of the cancer stem cell phenotype.
钙黏蛋白是上皮组织中细胞间黏附的介质。E-钙黏蛋白是一种已知的肿瘤抑制因子，在抑制癌细胞的侵袭表型中起核心作用。然而，N-钙黏蛋白和P-钙黏蛋白的异常表达（“钙黏蛋白转换”，CS）已被证明可促进癌症更具侵袭性和恶性的表型，P-钙黏蛋白可能是膀胱癌侵袭和转移的关键介质。钙黏蛋白还参与了许多与胚胎发育、组织形态发生和内环境稳定相关的信号事件。正是这些广泛的影响以及CS的严重影响，使得钙黏蛋白细胞黏附分子及其相关途径成为抑制癌症进展（包括膀胱癌）的有力候选靶点。本综述聚焦于膀胱癌背景下的CS，特别是向P-钙黏蛋白表达的转换，并讨论其他相关分子和现象，包括上皮细胞黏附分子（EpCAM）和癌症干细胞表型的发展。
