CNFS-FRE, IFR, Universite des Sciences et Technologies de Lille, Villeneuve d'Ascq, France.
Cancer Lett. 2010 May 1;291(1):59-66. doi: 10.1016/j.canlet.2009.09.017. Epub 2009 Oct 31.
Ovarian cancer is a highly metastatic disease and the leading cause of death from gynecologic malignancy. Hence, and understanding of the molecular changes associated with ovarian cancer metastasis could lead to the identification of targets for novel therapeutic interventions. The conversion of an epithelial cell to a mesenchymal cell plays a key role both in the embryonic development and cancer invasion and metastasis. Cells undergoing epithelial-mesenchymal transition (EMT) lose their epithelial morphology, reorganize their cytoskeleton and acquire a motile phenotype through the up- and down-regulation of several molecules including tight and adherent junctions proteins and mesenchymal markers. EMT is believed to be governed by signals from the neoplastic microenvironment including a variety of cytokines and growth factors. In ovarian cancer EMT is induced by transforming growth factor-beta (TGF-beta), epidermal growth factor (EGF), hepatocyte growth factor (HGF) and endothelin-1 (ET-1). Alterations in these cellular pathways candidate them as useful target for ovarian cancer treatment.
卵巢癌是一种高度转移性疾病,也是妇科恶性肿瘤死亡的主要原因。因此,了解与卵巢癌转移相关的分子变化可能有助于确定新的治疗干预靶点。上皮细胞向间充质细胞的转化在胚胎发育和癌症侵袭转移中都起着关键作用。上皮-间充质转化(EMT)过程中,细胞失去上皮形态,通过几种分子(包括紧密连接和黏附连接蛋白以及间充质标志物)的上调和下调重新组织细胞骨架并获得运动表型。EMT 被认为受到肿瘤微环境信号的调控,包括各种细胞因子和生长因子。在卵巢癌中,转化生长因子-β(TGF-β)、表皮生长因子(EGF)、肝细胞生长因子(HGF)和内皮素-1(ET-1)诱导 EMT。这些细胞通路的改变使它们成为卵巢癌治疗的有用靶点。