CAJ | 학술논문

目的:探讨赫赛汀对乳腺癌SK-BR3细胞Notch-1蛋白的影响及其作用机制,认识Notch-1信号通路在乳腺癌细胞形成赫赛汀耐药中的意义.方法:选用HER-2过表达乳腺癌SK-BR3细胞及HER-2非过表达乳腺癌MDA-MB-231细胞,免疫细胞化学法和Western blot 法检测两细胞株中Notch-1 蛋白的表达;应用赫赛汀处理SK-BR3 细胞,Western blot 法检测HER-2、Notch-1通路活性分子Notch-1IC的蛋白表达;RT-PCR法检测Notch-1靶基因HES-1 mRNA的表达;免疫共沉淀法检测SK-BR3细胞中Notch-1与HER-2是否存在相互作用.结果:Notch-1IC核定位水平及Notch-1IC蛋白表达水平在HER-2过表达乳腺癌细胞(9.37±0.64)中明显低于HER-2非过表达乳腺癌细胞(21.665±1.11),P＜0.01;赫赛汀处理SK-BR3细胞后,与未处理组比较,细胞内Notch-1IC蛋白及HES-1 mRNA水平均明显增高(P＜0.01,P＜0.01),HER-2蛋白表达水平在处理前后未发生明显变化(F=0.973,P＞0.05);免疫共沉淀结果显示Notch-1与HER-2蛋白之间存在共沉淀.结论:Notch-1蛋白在HER-2过表达乳腺癌细胞中活性下降;HER-2与Notch-1结合,可能负性调控Notch-1;赫赛汀活化的Notch-1信号通路,可能与细胞耐药发生有关.
목적:탐토혁새정대유선암SK-BR3세포Notch-1단백적영향급기작용궤제,인식Notch-1신호통로재유선암세포형성혁새정내약중적의의.방법:선용HER-2과표체유선암SK-BR3세포급HER-2비과표체유선암MDA-MB-231세포,면역세포화학법화Western blot 법검측량세포주중Notch-1 단백적표체;응용혁새정처리SK-BR3 세포,Western blot 법검측HER-2、Notch-1통로활성분자Notch-1IC적단백표체;RT-PCR법검측Notch-1파기인HES-1 mRNA적표체;면역공침정법검측SK-BR3세포중Notch-1여HER-2시부존재상호작용.결과:Notch-1IC핵정위수평급Notch-1IC단백표체수평재HER-2과표체유선암세포(9.37±0.64)중명현저우HER-2비과표체유선암세포(21.665±1.11),P＜0.01;혁새정처리SK-BR3세포후,여미처리조비교,세포내Notch-1IC단백급HES-1 mRNA수평균명현증고(P＜0.01,P＜0.01),HER-2단백표체수평재처리전후미발생명현변화(F=0.973,P＞0.05);면역공침정결과현시Notch-1여HER-2단백지간존재공침정.결론:Notch-1단백재HER-2과표체유선암세포중활성하강;HER-2여Notch-1결합,가능부성조공Notch-1;혁새정활화적Notch-1신호통로,가능여세포내약발생유관.