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RNAi干扰Ska2对H1299细胞增殖、迁移及侵袭能力的影响
引用本文:王义涛,蔡伟,朱远远,李溪月,张春冬,王森,雷云龙,张莹,朱慧芳,李轶,卜友泉.RNAi干扰Ska2对H1299细胞增殖、迁移及侵袭能力的影响[J].细胞生物学杂志,2014(5):624-630.
作者姓名:王义涛  蔡伟  朱远远  李溪月  张春冬  王森  雷云龙  张莹  朱慧芳  李轶  卜友泉
作者单位:[1]重庆医科大学生物化学与分子生物学教研室,重庆400016 [2]重庆医科大学分子医学与肿瘤研究中心,重庆400016
基金项目:国家自然科学基金(批准号:81171879、81302263)和重庆市科委自然科学基金(批准号:cstc2013jcyjA10043)资助的课题
摘    要:Ska2(spindle and kinetochore associated complex subunit2),又称FAM33A(family with sequence similarity33,member A),是新近发现的一个与细胞周期调控和肿瘤发生发展紧密相关的基瓯且与该团队前期发现的新基NPRR11(proline rich 11)共享一个双向启动子。但是,Ska2在肺癌中的具体作用和分子机制仍不清楚。该研究选用肺癌细胞系H1299,采用RNAi技术构建Ska2基因沉默的稳定细胞株,并进行了细胞表型和潜在分子机制分析。RT-PCR和Western blot结果表明,Ska2在mRNA和蛋白质水平上的表达均被有效抑制。细胞增殖、细胞迁移和侵袭实验结果表明,与对照细胞相比,Ska2基因沉默稳定细胞株的细胞增殖能力、细胞迁移和侵袭能力均显著降低。此外,Ska2基因被沉默后,CCNA1基因的表达显著下调。该研究的结果提示,Ska2与其对侧基因PRR11的功能高度相关,可能与PRR11共同参与肺癌细胞增殖、迁移和侵袭行为的调节。

关 键 词:Ska2  细胞增殖  肺癌  迁移  侵袭

The Effects of Ska2 Silencing on Cellular Proliferation,Migration and Invasion of H1299 Lung Cancer Cells
Wang Yitao,Cai Wei,Zhu Yuanyuan,Li Xiyue,Zhang Chundong,Wang Sen,Lei Yunlong,Zhang Ying,Zhu Huifang,Li Yi,Bu Youquan.The Effects of Ska2 Silencing on Cellular Proliferation,Migration and Invasion of H1299 Lung Cancer Cells[J].Chinese Journal of Cell Biology,2014(5):624-630.
Authors:Wang Yitao  Cai Wei  Zhu Yuanyuan  Li Xiyue  Zhang Chundong  Wang Sen  Lei Yunlong  Zhang Ying  Zhu Huifang  Li Yi  Bu Youquan
Institution:1Department of Biochemistry and Molecular Biology, Chongqing Medical University, Chongqing 400016, China; 2Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, China)
Abstract:Ska2 (spindle and kinetochore associated complex subunit 2), also known as FAM33A (family with sequence similarity 33, member A), is a recently identified gene involved in both cell cycle regulation and tumorigenesis, and it shares a bidirectional promoter with PRR11 (proline rich 11). In the present study, we utilized lung cancer cell line H1299 to construct Ska2-slienced cell strain by RNAi, and analyzed the cellular phenotype and potential molecular mechnism. The results of RT-PCR and Western blot revealed that Ska2 was efficiently silenced at both mRNA and protein levels. Phenotypic analysis revealed that the proliferation, migration and invasion activities were significantly inhibited in Ska2-silenced stable cell strain compared with those of the control cells. In addition, silencing of Ska2 resulted in the downregulation of CCNA1. Taken together, our results strongly suggested that Ska2 and its neighboring gene PRRll had similar functions and might play important roles in regulating the proliferation, migration and invasion of lung cancer cells.
Keywords:Ska2  cell proliferation  lung cancer  migration  invasion
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