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作 者:郑红[1] 张文玲[1] 王笑玉[2] 赵国强[2]
机构地区:[1]河南大学医学院,河南开封475004 [2]郑州大学基础医学院,河南郑州450052
出 处:《南方医科大学学报》2012年第12期1796-1799,共4页Journal of Southern Medical University
基 金:河南大学校内科研基金重点项目(2010ZRZD02)
摘 要:目的探讨人组织激肽释放酶10(KLK10)对舌癌Tca8113细胞增殖和侵袭力的影响。方法运用分子生物学技术,构建真核表达载体pIRES2-EGFP-KLK10,转染Tca8113细胞,分别用RT-PCR、Western blot检测KLK10 mRNA及蛋白表达水平。MTS细胞生长实验检测细胞增殖的变化;Transwell小室细胞侵袭实验检测细胞侵袭能力的变化。结果 pIRES2-EGFP-KLK10转染Tca8113细胞获得稳定细胞株,与空白对照组及空载体组比较,KLK10 mRNA及蛋白表达水平均明显增高,KLK10增强表达的舌癌细胞增殖和侵袭能力均明显减弱(P<0.05)。结论 KLK10表达增强能够降低人舌癌细胞的增殖和侵袭能力。KLK10基因可能成为肿瘤治疗上有前途的分子靶点。Objective To study the effect of kallikrein-related paptidase 10 (KLK10) on the proliferation and invasiveness of human tongue cancer cell line Tca8113. Methods The eukaryotic expression vector harboring KLK10 gene (pIRES2-EGFP-KLK10) was transfected in Tca8113 cells and the stable cell lines were selected by G418 screening. The mRNA and protein expression of KLK10 in transfected Tca8113 cells were assayed by RT-PCR and Western blotting, respectively, and the proliferation and invasiveness of the cells were evaluated by MTS cell growth assay and Transwell chamber invasion experiments. Results A stable Tca8113 cell line with high KLK10 expression was obtained, which showed significantly increased mRNA and protein expression levels of KLK10 and obviously attenuated proliferation and invasiveness compared with control and empty vector-transfected cells (P〈0.05). Conclusion Enhancing KLK10 gene expression can decrease the proliferation and invasiveness of human tongue cancer cells in vitro.
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