期刊文献+

肌球蛋白重链9在非小细胞肺癌恶性进展中的作用 被引量:1

Role of MYH9 in progression of non-small cell lung cancer
原文传递
导出
摘要 目的探索肌球蛋白重链9(MYH9)在非小细胞肺癌(NSCLC)恶性进展中的作用及其机制。方法使用实时荧光定量PCR检测60例NSCLC及癌旁正常组织中MYH9mRNA的表达水平,分析其表达水平与NSCLC临床特征之间的关系。用小干扰RNA干扰NSCLC细胞株NCI-H1975和NCI-H1299中MYH9的表达水平,使用CCK-8和Transwell侵袭系统检测干扰后细胞的增殖和侵袭情况。结果MYH9 mRNA在NSCLC中的表达水平高于癌旁正常组织(P<0.01),MYH9mRNA的表达与NSCLC的TNM分期相关(P<0.05)。干扰MYH9表达后,NCI-H1975和NCI-H1299细胞的增殖和侵袭能力下降(P<0.05)。p53mRNA在NSCLC中的表达与MYH9mRNA呈负相关(P<0.05),双荧光素酶报告基因系统显示,p53可结合MYH9启动子,抑制MYH9的表达。结论 MYH9受p53调控,其表达升高能促进NSCLC的恶性进展。 Objective To explore the role of myosin heavy chain 9(MYH9)in the progression of non-small cell lung cancer(NSCLC)and its mechanism.Methods The expressions of MYH9 mRNA in NSCLC and tumor-adjacent normal tissues were determined by real-time fluorescence quantitative PCR.The association of the expression level of MYH9 mRNA with clinical characteristics was analyzed.Small interference RNA was used to knock down the expression of MYH9 in NSCLC cell lines(NCI-H1975 and NCI-H1299).Cell proliferation and invasion were measured by CCK-8 assay and Transwell invasion assay,respectively.Results The expression of MYH9 mRNA in NSCLC tissues was higher than that in tumor-adjacent normal tissues(P<0.05),which was associated with TNM stage of NSCLC(P<0.05).Knock-down of MYH9 could suppress the proliferation and invasion of NSCLC cells(P<0.05).In addition,p53 mRNA expression was negatively correlated to MYH9 mRNA in NSCLC tissues(P<0.05).MYH9 promoter had potential binding sites for p53 using predicted bioinformatic analysis.Dual-luciferase reporter assay revealed that p53 could bind to the promoter of MYH9 and inhibit MYH9 expression.Conclusion MYH9 is regulated by p53 and promotes the progression of NSCLC.
作者 梁辰 陈刚 平国强 王静瑜 张炜明 LIANG Chen;CHEN Gang;PING Guoqiang(Department of Pathology,First Affliated Hospital,Nanjing Medical University, Nanjing 210029,CHINA)
出处 《江苏医药》 CAS 2019年第1期17-21,F0003,共6页 Jiangsu Medical Journal
关键词 肌球蛋白重链9 P53 非小细胞肺癌 Myosin heavy chain 9 p53 Non-small cell lung cancer
  • 相关文献

同被引文献7

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部