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作 者:王绍清[1] 吴甜[1] 帅智峰[1] 董海影[1] 张晓杰[1]
机构地区:[1]齐齐哈尔医学院病理教研室,黑龙江齐齐哈尔161006
出 处:《中华肿瘤防治杂志》2013年第10期737-740,共4页Chinese Journal of Cancer Prevention and Treatment
基 金:黑龙江省卫生厅科研课题(2010-231)
摘 要:目的:通过下调Lewis肺癌细胞中Vav3的表达,观察其对肺癌细胞体外迁移和侵袭能力的影响,探讨Vav3在肺癌转移过程中发挥的作用。方法:体外化学合成Vav3特异性siRNA(Vav3-163),并转染至Lewis肺癌细胞。蛋白质印迹法检测转染前后细胞中Vav3表达水平。Transwell小室实验观察下调Vav3对Lewis肺癌细胞体外迁移和侵袭能力的影响。结果:蛋白质印迹检测结果显示,转染Vav3-163序列后,Lewis肺癌细胞中Vav3的表达明显下调。实验组Vav3表达(0.112±0.005)低于LLC组(0.408±0.004)和对照组(0.388±0.005),F=22.052,P=0.002。下调Vav3在Lewis肺癌细胞中的表达后,迁移实验中干扰组穿过膜细胞数(31.0±10.5)明显少于Lewis肺癌细胞组(56.0±5.4)和对照组(49.0±9.1),F=11.213,P=0.002;体外侵袭实验中干扰组穿过人工基底膜细胞数(21.0±6.6)明显少于Lewis肺癌细胞组(59.0±9.8)和对照组(43.0±18.0),F=11.692,P=0.002。结论:下调Lewis肺癌细胞中Vav3的表达,具有抑制肺癌细胞体外迁移和侵袭能力的作用。OBJECTIVE: To observe the effect of small interference RNA (siRNA) mediated silencing of the vav3 on cell mi- gration and invasion ability in Lewis lung cancer cells. METHOIIS: Chemically synthesized siRNA targeting Vav3 (Vav3-163)was transfected into Lewis lung carcinoma cells. Western blotting were applied to detect the protein expression of Vav3. The migration and invasion of Lewis lung carcinoma cells in viro was measured by Transwell chamber assays. RESULTS: SiRNA of mouse Vav3-163 could inhibit the expression of Vav3. The protein level of Vav3 was decreased in Lewis lung cancer cells which transfected with Vav3-163 (0. 112±. 005) compared with the Lewis lung cancer cells (0. 408±0. 004) and control cells [(0. 388±0. 005),F= 22. 052, P=0. 002]. In migration experiment, the number of migration cells in siRNA group, Lewis lung cancer cell group and control group were (31.0± 10. 5), (56.0±5.4) and (49.0±9. 1) respectively,which were significantly different (F=11. 213,P=0. 002). In invasion experiment,the number of invasion cells in siRNA group (21.0± 6. 6) were lower compared with Lewis lung cancer cell group and control group [(59.0±9.8),(43.0±18. 0)],which were also significantly different (F=11. 692,P=0. 002). CONCLU- SION: Down-regulating the expression of Vav3 gene by siRNA can inhibit migration and invasion ability in Lewis lung cancer cells.
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