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中国癌症防治杂志 ›› 2020, Vol. 12 ›› Issue (2): 180-185.doi: 10.3969/j.issn.1674-5671.2020.02.13

• 基础研究 • 上一篇    下一篇

NKX6.3对食管癌细胞增殖、凋亡及侵袭的影响及作用机制

  

  1.  南充市中心医院, 川北医学院第二临床医学院,胸心外科,消化内科
  • 出版日期:2020-04-25 发布日期:2020-05-05
  • 基金资助:
    川北医学院科研发展计划项目(CBY18-A-YB24)

Effect of NKX6.3 on proliferation,apoptosis and invasion of esophageal cancer cells and its mechanism

  1. Department of Thoracic and Cardiovascular Surgery,Department of Gastroenterology, Nanchong City Central Hospital, the Second Clinical Medical College of North Sichuan Medical College Nanchong
  • Online:2020-04-25 Published:2020-05-05

摘要: 目的 探讨NKX6.3对食管癌细胞增殖、凋亡及侵袭的影响及可能的作用机制。方法 人食管癌EC9706细胞分别转染NKX6.3(NKX6.3组)和空白质粒(miR-NC组),设空白对照组(Control组)。CCK-8法检测细胞增殖情况,流式细胞仪检测细胞内活性氧、线粒体膜电位及细胞凋亡情况,Transwell 法检测细胞侵袭能力,Western blot检测增殖相关蛋白Ki67、侵袭相关蛋白(Vimentin、E-cadherin及N-cadherin),凋亡相关蛋白(Bcl-2、Bax及Caspase-3)的表达。结果 Control组、miR-NC组和NKX6.3组食管癌EC9706细胞中NKX6.3表达、细胞增殖能力、细胞内活性氧、线粒体膜电位、细胞凋亡及侵袭能力,以及Ki67、Vimentin、E-cadherin、N-cadherin、Bcl-2、Bax及Caspase-3蛋白表达差异均有统计学意义(P<0.01)。其中,NKX6.3组NKX6.3表达量、细胞内活性氧,细胞凋亡率,Vimentin、E-cadherin、Bax及Caspase-3蛋白表达水平较miR-NC组升高;而线粒体膜电位、细胞增殖率、细胞侵袭数目、N-cadherin及Bcl-2蛋白表达水平降低(P<0.01)。结论 NKX6.3可抑制食管癌细胞增殖和侵袭,促进细胞凋亡,该作用可能通过调控食管癌细胞中的增殖凋亡相关蛋白表达及活性氧水平实现。

关键词: 食管癌, NKX6.3, 活性氧, 增殖, 凋亡, 侵袭

Abstract: Objective To investigate the effect of NKX6.3 on proliferation,apoptosis,and invasion of esophageal cancer cells and its possible mechanism. Methods Human esophageal cancer EC9706 cells were transfected and divided into NKX6.3 group(transfected with NKX6.3),miR-NC group(transfected with blank plasmid) and blank control group(Control group). CCK-8 method was used to detect cell proliferation,the flow cytometry was applied to detect intracellular reactive oxygen species,mitochondrial membrane potential and apoptosis of esophageal cancer cells,and Transwell method was applied to detect invasion of esophageal cancer cells. Expression of proliferation-related protein(Ki67),invasion-related proteins(Vimentin,E-cadherin,and N-cadherin) and apoptosis-related proteins(Bcl-2,Bax,and Caspase-3) were detected by Western blot. Results Statistically significant difference(P<0.01) existed among the Control group,miR-NC group and the expression of NKX6.3 in EC9706 cell in NKX6.3 group,cell proliferation capacity,intracellular reactive oxygen species,mitochondrial membrane potential,cell apoptosis and invasion of esophageal cancer cells,as well as in the expression of Ki67,Vimentin,E-cadherin,N-cadherin,Bcl-2,Bax and Caspase-3 proteins. The expression of NKX6.3,intracellular reactive oxygen species,apoptosis rate,and Vimentin,E-cadherin,Bax and Caspase-3 proteins expression in the NKX6.3 group were significantly higher than those in the miR-NC group,while mitochondrial membrane potential,cell proliferation rate,cell invasion number,and the expression of N-cadherin and Bcl-2 proteins were significantly lower(P<0.01). Conclusion NKX6.3 can inhibit the proliferation and invasion of esophageal cancer cells and promote cell apoptosis,probably through regulating the expression of proliferation-related proteins and the level of reactive oxygen species in esophageal cancer cells.

Key words: Esophageal cancer, NKX6.3, Reactive oxygen species, Proliferation, Apoptosis, Invasion

中图分类号: 

  • R735.1