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Role of epithelial-mesenchymal transition in gastric cancer initiation and progression

机译:上皮-间质转化在胃癌发生和发展中的作用

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Gastric cancer is one of the most common malignant tumors worldwide. Due to its intricate initiation and progression mechanisms, early detection and effective treatment of gastric cancer are difficult to achieve. The epithelial-mesenchymal transition (EMT) is characterized as a fundamental process that is critical for embryonic development, wound healing and fibrotic disease. Recent evidence has established that aberrant EMT activation in the human stomach is closely associated with gastric carcinogenesis and tumor progression. EMT activation endows gastric epithelial cells with increased characteristics of mesenchymal cells and reduces their epithelial features. Moreover, mesenchymal cells tend to dedifferentiate and acquire stem cell or tumorigenic phenotypes such as invasion, metastasis and apoptosis resistance as well as drug resistance during EMT progression. There are a number of molecules that indicate the stage of EMT (e.g., E-cadherin, an epithelial cell biomarker); therefore, certain transcriptional proteins, especially E-cadherin transcriptional repressors, may participate in the regulation of EMT. In addition, EMT regulation may be associated with certain epigenetic mechanisms. The aforementioned molecules can be used as early diagnostic markers for gastric cancer, and EMT regulation can provide potential targets for gastric cancer therapy. Here, we review the role of these aspects of EMT in gastric cancer initiation and development. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved.
机译:胃癌是全世界最常见的恶性肿瘤之一。由于其复杂的起始和进展机制,难以实现对胃癌的早期检测和有效治疗。上皮-间质转化(EMT)被认为是对胚胎发育,伤口愈合和纤维化疾病至关重要的基本过程。最近的证据表明,人胃中异常的EMT激活与胃癌的发生和肿瘤的发展密切相关。 EMT激活赋予胃上皮细胞增加间充质细胞的特性并降低其上皮特性。此外,间充质细胞倾向于去分化并获得干细胞或致瘤表型,例如在EMT进展过程中的侵袭,转移和凋亡抗性以及药物抗性。有许多分子指示EMT的阶段(例如,E-钙黏着蛋白,一种上皮细胞生物标志物);因此,某些转录蛋白,尤其是E-钙粘蛋白转录阻遏物,可能参与EMT的调控。此外,EMT调节可能与某些表观遗传机制有关。前述分子可以用作胃癌的早期诊断标记,并且EMT调节可以为胃癌治疗提供潜在的靶标。在这里,我们回顾了EMT这些方面在胃癌的发生和发展中的作用。 (C)2014百事登出版集团有限公司。版权所有。

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