中华肿瘤杂志
中華腫瘤雜誌
중화종류잡지
CHINESE JOURNAL OF ONCOLOGY
2013年
2期
94-97
,共4页
张敏%牟晓燕%姜淑娟%刘庆亮%李道卫
張敏%牟曉燕%薑淑娟%劉慶亮%李道衛
장민%모효연%강숙연%류경량%리도위
肺肿瘤%表皮生长因子受体%RNA,双链%放射敏感性
肺腫瘤%錶皮生長因子受體%RNA,雙鏈%放射敏感性
폐종류%표피생장인자수체%RNA,쌍련%방사민감성
Lung neoplasms%Epidermal growth factor receptor%RNA,double-stranded%Radiosensitivity
目的 探讨表皮生长因子受体(EGFR)表达与非小细胞肺癌(NSCLC)放疗敏感性的关系.方法 体外化学合成EGFR基因序列特异性双链RNA(dsRNA)结合脂质体Lipofectamine 2000转染肺腺癌细胞株SPC-A1,采用实时荧光定量PCR(real-time PCR)和Western blot法测定转染细胞中EGFRmRNA和蛋白的表达,采用集落抑制实验观察EGFR序列特异性dsRNA(dsRNA-EGFR)的体外放疗增敏作用.建立裸鼠肿瘤模型,通过测定肿瘤体积和肿瘤重量,绘制肿瘤生长曲线,计算肿瘤抑制率.结果 对照组、dsRNA-unrelated组和dsRNA-EGFR组的EGFRmRNA相对表达量分别为1.51±0.22、1.38±0.15和0.45±0.11(F=482.7,P＜0.01),EGFR蛋白表达水平分别为2340.87±10.99、2231.85 ±35.66和832.03±39.13(F =263.3,P＜0.05).dsRNA-EGFR可将对照组EGFR mRNA和蛋白水平分别下调70.2％和64.5％.放疗对照组、dsRNA-unrelated联合放疗组和dsRNA-EGFR联合放疗组的集落抑制率分别为9.3％、12.5％和65.5％,肿瘤抑制率分别为21.3％、24.4％和64.2％,dsRNA-EGFR联合放疗可显著抑制体外、体内的肿瘤生长.结论 dsRNA-EGFR可显著抑制NSCLC中EGFR mRNA和蛋白的表达,有效抑制肿瘤生长,增强NSCLC的放疗敏感性.
目的 探討錶皮生長因子受體(EGFR)錶達與非小細胞肺癌(NSCLC)放療敏感性的關繫.方法 體外化學閤成EGFR基因序列特異性雙鏈RNA(dsRNA)結閤脂質體Lipofectamine 2000轉染肺腺癌細胞株SPC-A1,採用實時熒光定量PCR(real-time PCR)和Western blot法測定轉染細胞中EGFRmRNA和蛋白的錶達,採用集落抑製實驗觀察EGFR序列特異性dsRNA(dsRNA-EGFR)的體外放療增敏作用.建立裸鼠腫瘤模型,通過測定腫瘤體積和腫瘤重量,繪製腫瘤生長麯線,計算腫瘤抑製率.結果 對照組、dsRNA-unrelated組和dsRNA-EGFR組的EGFRmRNA相對錶達量分彆為1.51±0.22、1.38±0.15和0.45±0.11(F=482.7,P＜0.01),EGFR蛋白錶達水平分彆為2340.87±10.99、2231.85 ±35.66和832.03±39.13(F =263.3,P＜0.05).dsRNA-EGFR可將對照組EGFR mRNA和蛋白水平分彆下調70.2％和64.5％.放療對照組、dsRNA-unrelated聯閤放療組和dsRNA-EGFR聯閤放療組的集落抑製率分彆為9.3％、12.5％和65.5％,腫瘤抑製率分彆為21.3％、24.4％和64.2％,dsRNA-EGFR聯閤放療可顯著抑製體外、體內的腫瘤生長.結論 dsRNA-EGFR可顯著抑製NSCLC中EGFR mRNA和蛋白的錶達,有效抑製腫瘤生長,增彊NSCLC的放療敏感性.
목적 탐토표피생장인자수체(EGFR)표체여비소세포폐암(NSCLC)방료민감성적관계.방법 체외화학합성EGFR기인서렬특이성쌍련RNA(dsRNA)결합지질체Lipofectamine 2000전염폐선암세포주SPC-A1,채용실시형광정량PCR(real-time PCR)화Western blot법측정전염세포중EGFRmRNA화단백적표체,채용집락억제실험관찰EGFR서렬특이성dsRNA(dsRNA-EGFR)적체외방료증민작용.건립라서종류모형,통과측정종류체적화종류중량,회제종류생장곡선,계산종류억제솔.결과 대조조、dsRNA-unrelated조화dsRNA-EGFR조적EGFRmRNA상대표체량분별위1.51±0.22、1.38±0.15화0.45±0.11(F=482.7,P＜0.01),EGFR단백표체수평분별위2340.87±10.99、2231.85 ±35.66화832.03±39.13(F =263.3,P＜0.05).dsRNA-EGFR가장대조조EGFR mRNA화단백수평분별하조70.2％화64.5％.방료대조조、dsRNA-unrelated연합방료조화dsRNA-EGFR연합방료조적집락억제솔분별위9.3％、12.5％화65.5％,종류억제솔분별위21.3％、24.4％화64.2％,dsRNA-EGFR연합방료가현저억제체외、체내적종류생장.결론 dsRNA-EGFR가현저억제NSCLC중EGFR mRNA화단백적표체,유효억제종류생장,증강NSCLC적방료민감성.
Objective To explore the relationship between epidermal growth factor receptor(EGFR) gene expression and radiosensitivity of non-small-cell lung cancer (NSCLC) cells.Methods EGFR sequence-specific double-stranded RNA (dsRNA-EGFR) was chemically synthesized.NSCLC cell line SPC-A1 was transfected with dsRNA-EGFR formulated with Lipefectamine 2000.Western blot and real-time PCR were used to determine the EGFR mRNA and protein expression,respectively.Colony inhibition test was adopted to observe the radiosensitizing effect.To establish the nude mouse tumor models,calculate the tumor growth inhibition rate and make the tumor growth curve by measuring its size and weight.Results EGFR mRNA levels were 1.51 ±0.22,1.38 ±0.15 and 0.45 ±0.11 in the control group,dsRNA-unrelated group and dsRNA-EGFR group,respectively (F =482.7,P ＜0.01).The contents of EGFR protein were 2340.87 ± 10.99,2231.85 ±35.66 and 832.03 ±39.13 in the control group,dsRNA-unrelated group and dsRNA-EGFR group,respectively (F =263.3,P ＜0.05).Compared with the control group,dsRNA-EGFR sequence specifically decreased the expressions of EGFR mRNA by 70.2％ and EGFR protein by 64.5％.The colony inhibition rates of the control group,dsRNA-unrelated combined with radiotherapy group and dsRNA-EGFR combined with radiotherapy group were 9.3％,12.5％ and 65.5％,and the tumor growth inhibition rates were 21.3％,24.4％ and 64.2％,respectively.The combination of dsRNA-EGFR and radiotherapy significantly inhibited the tumor growth in vitro and in vivo.Conclusions DsRNA-EGFR shows an apparent inhibitory effect on the expression of EGFR mRNA and protein of NSCLC cells,effectively inhibit the tumor growth in vivo,and enhance the radiosensitivity of NSCLC.
