组蛋白赖氨酸残基去甲基化酶4B过表达对乳腺癌细胞MCF-7侵袭迁移能力的影响

The effect of lysine（K）-specific demethylase 4B overexpression on the invasion and migration ability of breast cancer cell MCF-7

目的 构建组蛋白赖氨酸残基去甲基化酶4B（KDM4B）过表达乳腺癌细胞株MCF-7,观察KDM4B对MCF-7侵袭迁移能力的影响,并探索其机制.方法 利用KDM4B慢病毒感染乳腺癌细胞株MCF-7,筛选KDM4B过表达稳定细胞株,Western blot法检测MCF-7细胞中KDM4B基因蛋白表达;迁移实验、侵袭实验观察过表达KDM4B对乳腺癌MCF-7细胞迁移和侵袭能力的影响;Western blot法检测细胞上皮-间充质转化相关蛋白E-钙黏蛋白（E-cadherin）、波形蛋白（Vimentin）表达.结果 Western blot法验证过表达KDM4B的乳腺癌细胞株MCF-7构建成功;迁移实验中过表达KDM4B细胞穿膜数目[（94±8）个]较对照组[（36±6）个]明显增多,侵袭实验中过表达KDM4B细胞穿膜数目[（18±2）个]较对照组[（5±1）个]明显增多,差异均有统计学意义（P＜0.01）;过表达KDM4B细胞中E-cadherin表达量较对照组明显降低,Vimentin表达量较对照组明显增高.结论 过表达KDM4B基因可促进乳腺癌细胞株MCF-7上皮-间充质转化过程,并提高细胞迁移、侵袭能力.

Objective To construct lentivirus-induced lysine （K）-specific demethylase 4B （KDM4B） overexpression breast cancer cell MCF-7 and observe the effect of KDM4B on the invasion and migration ability of breast cancer cell MCF-7,and explore the underlying mechanism.Methods Lentivirus-induced KDM4B over-expression was used for in vitro function analyses in breast cancer cell line MCF-7,including migration and invasion assay,and Western blotting assay.Results Compared to the control,the expression of KDM4B was significantly increased in the experimental group,while the expression of E-cadherin was significantly decreased and Vimentin was significantly increased.In the migration assay,the number of penetrating the membrane was markedly increased in the experimental group as campared with the control （94 ± 8 vs.36± 6）.The same phenomenon was also found in the invasion assay （18 ± 2 vs.5 ± 1）.Conclusion Up-regulation of KDM4B could promote the process of epithelial-mesenchymal transition,migration and invasion of breast cancer cell line MCF-7.