【摘 要】
：
The mechanism accounting for metastasis in prostate cancer is not well understood.Transition of cancer cells to a metastatic phenotype within the primary tumor site may involve the loss of the epithel
【机 构】
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Department of Medicine Stony Brook University USA
【出 处】
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BIT‘s2nd Annual World Cancer Congess-2009 (2009第二届癌症大会)
论文部分内容阅读
The mechanism accounting for metastasis in prostate cancer is not well understood.Transition of cancer cells to a metastatic phenotype within the primary tumor site may involve the loss of the epithelial phenotype and the acquisition of a mesenchymal phenotype (epithelial-mesenchymal transition: EMT).Experimental models and clinical correlations of different types of cancers have implicated numerous mechanistic factors in EMT.We have reported that the signaling pathways involved in MT1-MMP induced EMT include the Wnt5a and Rac 1 pathways (J.Biol.Chem.2008; 283:6232), and, most recently, the generation of reactive oxygen species (ROS).Expression of MT1-MMP in human LNCaP prostate cancer cells induces EMT-like phenotypic changes associated with loss of E-eadherin at the primary tumor site.Using cDNA microarray and shRNA strategies, we demonstrated that Wnt5a is a downstream effector of MT1-MMP induced EMT.To explore the participation of ROS in EMT, a stable clone of MT1-MMP transfected LNCaP cells was compared to vector-transfected LNCaP cells in regard to generation of ROS.
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