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dal1基因蛋白表达及其点突变1810ct575cystyr与非小细胞肺癌转移关系word格式论文
The Association of DAL-1 Protein Expressi- on and Point Mutation (1810 CT/575Cys Tyr) with the Metastasis of None Small Cell Lung CancersAbstractObjectiveLung cancer is one of the most common malignancies , among which 80%~ 85% are NSCLC. The direct cause of treatment failure and the vast majority of patient death are the invasion and metastasis of tumor. Thus, it becomes an urgent issue to seek out metastasis- related genes and its molecular targets of lung cancer at present.DAL-1 is a member of 4.1family, which expressed reducely or negatively in many type tumors such as NSCLC, breast cancer and meningiomas [1-4]. Reexpressed DAL-1 in NSCLC and breast cancer cells can inhibit them reproduction [1,5], suggest that protein DAL-1 may be a tumor suppressor.DAL-1 located at cell membrane by immunochemistry assay, and mainly focuses on the junction between cells, distributed as “honeycomb” [1]. Charboneau AL. et al. [6] find that DAL-1 expression enhances the attachment between breast cancer cells. Our pre-experiment in vitro show that silent the expression of DAL-1 can enhance migration and mobility of NSCLC cell [7]. We speculate that the loss of DAL-1 expression may weaken the connection and adhension between cells so that tumor cells detach and migrate easly. Therefore, we detected the protein expression of DAL-1 of human tissue, and further test the the association of it with the metastasis ofNSCLC.Mechanisms of gene inactivation include genetic mechanisms such as gene deletion and mutation and epigenetic mechanisms such as DNA methylation and change in chromatin conformation. Our Preliminary studies suggest that, loss of DAL-1 expression is mainly caused by the methylation of promoter [7]. But part of tumors in which DAL-1 expressed negative hadn’t the methylation of DAL-1 promoter. We suppose that there be some other causes that lead to the loss of DAL-1 expression. Point mutation is one of the common causes of gene loss. The current studies suggest that there ar
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