现代肿瘤医学
現代腫瘤醫學
현대종류의학
JOURNAL OF MODERN ONCOLOGY
2014年
10期
2259-2262
,共4页
李紫璇%钟红珊%徐克%邱雪杉
李紫璇%鐘紅珊%徐剋%邱雪杉
리자선%종홍산%서극%구설삼
丝裂原诱导基因%EGFR%增殖
絲裂原誘導基因%EGFR%增殖
사렬원유도기인%EGFR%증식
Mig-6%EGFR%proliferation
目的:观察Mig-6在非小细胞肺癌组织中的表达及其与EGFR表达的关系。在肺癌细胞系中探讨上、下调Mig-6表达后细胞增殖能力及 EGFR通路的变化。方法:用免疫组化,蛋白免疫印迹及实时定量PCR的方法检测肺癌及癌旁组织中Mig-6及EGFR的表达。在肺癌细胞系中通过使用Mig-6质粒和小干扰RNA分别上调和下调Mig-6,CCK-8法检测两株细胞系增殖能力,蛋白免疫印迹检测细胞中p-EG-FR、p-EGFR及p-AKT表达水平。结果:Mig-6在非小细胞肺癌组织中低表达(51.6%),并与EGFR表达呈负相关( P=0.003)。在肺癌细胞系中,上调Mig-6表达可以抑制细胞增殖并抑制EGFR、ERK及AKT的磷酸化,下调Mig-6表达则能促进细胞增殖并促进EGFR、ERK及AKT的磷酸化。结论:Mig-6表达在肺癌中与EGFR呈负相关,在肺癌细胞系中Mig-6通过负向调控EGFR下游通路而抑制细胞增殖。
目的:觀察Mig-6在非小細胞肺癌組織中的錶達及其與EGFR錶達的關繫。在肺癌細胞繫中探討上、下調Mig-6錶達後細胞增殖能力及 EGFR通路的變化。方法:用免疫組化,蛋白免疫印跡及實時定量PCR的方法檢測肺癌及癌徬組織中Mig-6及EGFR的錶達。在肺癌細胞繫中通過使用Mig-6質粒和小榦擾RNA分彆上調和下調Mig-6,CCK-8法檢測兩株細胞繫增殖能力,蛋白免疫印跡檢測細胞中p-EG-FR、p-EGFR及p-AKT錶達水平。結果:Mig-6在非小細胞肺癌組織中低錶達(51.6%),併與EGFR錶達呈負相關( P=0.003)。在肺癌細胞繫中,上調Mig-6錶達可以抑製細胞增殖併抑製EGFR、ERK及AKT的燐痠化,下調Mig-6錶達則能促進細胞增殖併促進EGFR、ERK及AKT的燐痠化。結論:Mig-6錶達在肺癌中與EGFR呈負相關,在肺癌細胞繫中Mig-6通過負嚮調控EGFR下遊通路而抑製細胞增殖。
목적:관찰Mig-6재비소세포폐암조직중적표체급기여EGFR표체적관계。재폐암세포계중탐토상、하조Mig-6표체후세포증식능력급 EGFR통로적변화。방법:용면역조화,단백면역인적급실시정량PCR적방법검측폐암급암방조직중Mig-6급EGFR적표체。재폐암세포계중통과사용Mig-6질립화소간우RNA분별상조화하조Mig-6,CCK-8법검측량주세포계증식능력,단백면역인적검측세포중p-EG-FR、p-EGFR급p-AKT표체수평。결과:Mig-6재비소세포폐암조직중저표체(51.6%),병여EGFR표체정부상관( P=0.003)。재폐암세포계중,상조Mig-6표체가이억제세포증식병억제EGFR、ERK급AKT적린산화,하조Mig-6표체칙능촉진세포증식병촉진EGFR、ERK급AKT적린산화。결론:Mig-6표체재폐암중여EGFR정부상관,재폐암세포계중Mig-6통과부향조공EGFR하유통로이억제세포증식。
Objective:To observe the expression of Mig-6 in non small cell lung cancer( NSCLC)and its rela-tionship with EGFR,and study the proliferation ability and EGFR pathway change in NSCLC cell line . Methods:Immunohistochemistry ,Western blot and real time PCR were used to detect the expression of Mig-6 and EGFR in NSCLC. In lung cancer cell we used Mig-6 plaimid to up-regulate Mig-6,siMig-6 method to down regulate Mig-6,the CCK-8 assy was used to detect the proliferation of both two cell lines,Western blot to detect the expres-sion of p-EGFR,p-EGFR and p-AKT in transfectioned A549 and BE1 cell line. Results:The expression of Mig-6 was down-regulated in NSCLC,it was negatively correlated with the expression of EGFR(P=0. 003). Up-reg-ulation of Mig-6 can inhibit the proliferation of A549 cell and the expression of p-EGFR,p-EGFR and p-AKT. Down-regulation of Mig-6 in BE1 by siRNA can prompt the proliferation ablity,and the expression of p-EGFR,p-EGFR and p-AKT were also increased. Conclusion:Mig-6 expression in lung cancer was negatively correlated with EGFR. In lung cancer cell lines Mig-6 can inhibit cell proliferation possibly through inhibition of EGFR down-stream pathways.