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siRNA沉默KLF4表达促进HeLa细胞迁移与增殖

Silencing the Expression of KLF4 by siRNA Improves the Migration and Proliferation of HeLa Cells
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摘要 目的:研究Krüppel样因子4(KLF4)的表达下调对HeLa细胞迁移与增殖的影响。方法:设计合成针对KLF4的si RNA和阴性对照si RNA,并转染至HeLa细胞中。使用含有10 ng/m L TGF-β1和10%胎牛血清的DMEM培养液诱导HeLa细胞发生上皮间质转化,对照组使用不含TGF-β1的培养液。通过Transwell迁移实验和划痕实验观察HeLa细胞迁移变化;通过细胞增殖实验和流式细胞术观察HeLa细胞增殖状况和细胞周期分布。结果:转染了si RNA的HeLa细胞经TGF-β1诱导后,其细胞迁移能力较其他各组显著提高;与转染了阴性对照si RNA和空白对照的细胞相比,转染si RNA的HeLa细胞增殖能力明显提高;TGF-β1可以使HeLa细胞周期发生G1期阻滞,但是采用si RNA干扰KLF4的表达对此过程无明显影响。结论:使用si RNA下调KLF4的表达可以促进HeLa细胞的迁移与增殖。 Objective: To investigate the effect of KLF4 expression downregulation on the migration and proliferation of HeLa cells. Methods: siRNA targeted to KLF4 and control siKNA were designed and transfected into the HeLa cells. DMEM with 10ng/ml TGF-β1 and 10% fetal calf serum (FBS) was used to induce the epithelial mesenchymal transition of HeLa. Culture medium without TGF-β1 was taken as control. The migration of HeLa cells were observed by Transwell and scratch wound assay. The proliferation and cell cycle of HeLa cells were detected by proliferation assay and Flow Cytometry. Results: Compared with other groups, the migration of HeLa cells were improved greatly after being transfected by siRNA-KLF4 and induced by TGF-β1. The proliferation of HeLa cells transfected by siRNA-KLF4 were obviously increased compared with the cells transfected by control siRNA and blank control. TGF-β1 could induce G1 block of HeLa cell cycle, but the downregnlation of KLF4 showed no obvious effects. Conclusion: Downregnlation of the KLF4 expression by siRNA obviously improve the migration and proliferation of HeLa cells.
出处 《现代生物医学进展》 CAS 2017年第32期6228-6231,6270,共5页 Progress in Modern Biomedicine
基金 国家自然科学基金项目(81301921) 陕西省自然科学基金项目(2013JM4023)
关键词 Krfippel样因子4 HELA细胞 迁移 增殖 转化生长因子-Β1 KLF4 HeLa cells Migration Proliferation TGF-β1
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  • 1Savagner P,Boyer B, Valles AM, et al. Modulations of the epithelial phenotype during embryogenesis and cancer pro- gression [ J ]. Cancer Treat Res, 1994,71:229-249.
  • 2Thompson EW, Torri J, Sabol M, et al. Oncogene-induced basement membrane invasiveness in human mammary epi- thelial cells [ J 1- Clin Exp Metastasis, 1994,12 ( 3 ) : 181 - 194.
  • 3Cui J, Shi M, Quan M,et al. Regulation of EMT by KLF4 in gastrointestinal cancer [ J]. Curr Cancer Drug Targets, 2013,13 (9) :986-995.
  • 4Huang CC, Liu Z, Li X, et al. KLF4 and PCNA identify stages of tumor initiation in a conditional model of cutane- ous squamous epithelial neoplasia [ J ]. Cancer Biol Ther, 2005,4(12) : 1401-1408.
  • 5Segre JA, Bauer C, Fuchs E. Klf4 is a transcription factor required for establishing the barrier function of the skin [ J]. Nat Genet, 1999,22(4) :356-360.
  • 6Xiao W,Zhou S,Xu H,et al. Nogo-B promotes the epithe- lial-mesenchymal transition in HeLa cervical cancer cells via Fibulin-5 [ J ]. Oncol Rep,2013,29 ( 1 ) : 109-116.
  • 7Lee MY, Chou CY,Tang MJ, et al. Epithelial-mesenchymal transition in cervical cancer: correlation with tumor pro- gression, epidermal growth factor receptor overexpression, and snail up-regulation [ J ]. Clin Cancer Res, 2008, 14 ( 15 ) :4743-4750.
  • 8Yang J, Weinberg RA. Epithelial-mesenchymal transition: at the crossroads of development and tumor metastasis [ J ]. Dev Cell, 2008,14 ( 6 ): 818-829.
  • 9Liang X. EMT : new signals from the invasive front [ J ]. O- ral Oneo1,2011,47 ( 8 ) :686-687.
  • 10Christofori G. New signals from the invasive front [ J ]. Nature, 2006,441 (7092) :444-450.

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