期刊文献+

FAM216B通过抑制AKT通路磷酸化抑制非小细胞肺癌的侵袭转移 被引量:2

FAM216B inhibition of invasion and metastasis of non-small cell lung cancer by inhibiting phosphorylation of AKT pathway
原文传递
导出
摘要 目的研究FAM216B是否通过抑制AKT磷酸化抑制上皮间质转化进而探讨其对非小细胞肺癌增殖侵袭能力的影响。方法应用基因表达谱数据动态分析数据库、生存分析数据库分析FAM216B与非小细胞肺癌患者预后影响。免疫组织化学染色方法检测FAM216B在肺癌患者中的表达,蛋白质免疫印迹方法检测神经钙粘蛋白、上皮细胞钙粘附蛋白、磷酸化蛋白激酶B的表达,克隆形成实验检测FAM216B过表达后肿瘤细胞增殖能力的影响。结果FAM216B高表达肺癌患者预后良好,FAM216B在肺癌组织中明显低表达,FAM216B过表达抑制肿瘤细胞增殖能力,FAM216B过表达抑制AKT通路磷酸化,FAM216B过表达抑制上皮间质转化。结论FAM216B通过AKT信号通路抑制上皮间质转化继而抑制非小细胞肺癌的演进。 Objective To investigate whether FAM216 B inhibits epithelial mesenchymal transition by inhibiting Akt phosphorylation,and to explore its effect on the proliferation and invasion of non-small cell lung cancer.Methods Between the prognostic effects of FAM216 B and non-small cell lung cancer patients were analyzed by using gene expression profile data dynamic analysis database and survival analysis database.Immunohistochemical staining was used to detect the expression of FAM216 B in lung cancer patients.Western blotting was used to detect the expression of neurocadherin,epithelial cadherin and phosphorylated protein kinase B.the effect of FAM216 B overexpression on the proliferation of tumor cells was detected by clone formation assay.Results The prognosis of lung cancer patients with high expression of FAM216 B was good,and the expression of FAM216 B was lower significantly in lung cancer than in normal lung tissues.The overexpression of FAM216 B inhibited the proliferation of tumor cells,the phosphorylation of Akt,and epithelial mesenchymal transition.Conclusion FAM216 B inhibits epithelial mesenchymal transition through Akt signaling pathway,and then inhibits the evolution of non-small cell lung cancer.
作者 栗境铎 郭映雪 侯再昱 苗原 LI Jing-duo;GUO Ying-xue;HOU Zai-yu;Miao Yuan(Department of Pathology,China Medical University,Shenyang 110001,China)
出处 《解剖科学进展》 2020年第5期579-582,共4页 Progress of Anatomical Sciences
基金 国家自然科学基金(81472805)。
关键词 非小细胞肺癌 磷酸化蛋白激酶B 上皮间质转化 增殖 NSCLC p-AKT EMT proliferation
  • 相关文献

参考文献1

同被引文献16

二级引证文献6

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