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作 者:陈周浔[1] 周宏众[1] Henning Dralle Cuong Hoang-Vu
机构地区:[1]温州医科大学附属第一医院胃肠外科,浙江温州325015 [2]德国Martin-Luther-University,Halle-Wittenberg普通,内脏,血管外科中心外科,外科肿瘤与实验研究组,德国哈雷06102
出 处:《温州医学院学报》2015年第5期346-349,353,共5页Journal of Wenzhou Medical College
基 金:温州市科技局科研基金资助项目(2014Y0195)
摘 要:目的:探讨肿瘤转移抑制因子CD82在调控人甲状腺癌细胞侵润和迁移中的作用以及发挥作用的相关分子机制。方法:采用基因工程技术,将含CD82全长基因的p CDNA3.1质粒用于细胞转染,构建过表达CD82基因的FTC-133细胞株,并将其与野型FTC-133细胞株进行生物性状比对。利用MTT法及Transwell细胞迁移实验检测CD82对FTC-133细胞侵润和迁移能力的影响。结果:与野生型或者空质粒转染细胞相比,各转染细胞(clone 1、2、3)在转染后24、48及72 h的增殖率减少(P>0.05);与野生型或者空质粒转染细胞相比,各转染细胞(clone 1、2、3)在转染后24、48及72 h的迁移能力明显减少(P<0.05)。结论:CD82可以明显降低FTC-133细胞的增殖及侵袭能力,与甲状腺癌发展与进程密切相关。Objective: To study the role of tumor suppressor gene CD82 in the regulation of thyroid carcinoma cell invasion/migration and its related molecular mechanisms. Methods: By using genetic engineering technology, the plasmid p CDNA3.1, which reconsturcted with the full length CD82 gene, was transfected into the thyroid carcinoma FTC-133 cells. By MTT and Transwell Assays, the proliferation rate and migration ability of these high expressed CD82 FTC-133 cells were compared with the wild-type cells FTC-133 cells. Results: 24, 48, 72 hours after transfection, the transfected cells showed reduced proliferation rate(P〉0.05) and significant lower migration ability(P〈0.05) in comparison with the wild-type cells and mock cells(trasfected with empty plasmid). Conclusion: These results illustrate that CD82 can reduce FTC-133 cell proliferation and invasiveness, CD82 is closely related to development and progression of thyroid carcinoma.
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