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细胞上皮-间质转变(epithelial-mesenchymal transition,EMT),与肿瘤的局部浸润以及远处转移有着非常密切的关系。肿瘤细胞EMT的发生包括诸多因素,主要有转录因子表达上调以及信号通路[如磷脂酰肌醇3-激酶(phosphatidyl inositol-3kinase,PI3K)/蛋白激酶B(protein kinase B,PKB,又称AKT)通路和Ras/丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)通路等]开启等,从而促使细胞间黏附力下降,失去了上皮细胞的顶底极性,并伴随细胞形态的改变。其中E-钙黏着糖蛋白(E-cadherins,E-cad)的表达下调或沉默是EMT发生的重要标志。本文就肿瘤细胞EMT发生机制的最新研究进展作一综述。
Epithelial-mesenchymal transition (EMT) is closely related to the local invasion of tumor and distant metastasis. The occurrence of EMT in tumor cells includes many factors, including the up-regulation of transcription factors and the signaling pathways [such as phosphatidylinositol-3kinase (PI3K) / protein kinase B (PKB) Pathways and the mitogen-activated protein kinase (MAPK) pathway, etc.) to open and so on, thereby contributing to the decline in intercellular adhesion, loss of epithelial top and bottom epithelial polarity, accompanied by changes in cell morphology. Among them, the down-regulation or silencing of E-cadherin (E-cad) expression is an important marker of EMT. This article reviews the latest research progress of tumor cell EMT mechanism.