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作 者:郑蕊[1] 邢小飞[1] 靳飞[1] 陈海丽[1] Zheng Rui;Xing Xiaofei;Jin Fei;Chen Haili(Clinical Laboratory,Zhengzhou No.7 People’s Hospital,Zhengzhou 450000,China)
出 处:《中国组织化学与细胞化学杂志》2021年第6期540-544,551,共6页Chinese Journal of Histochemistry and Cytochemistry
摘 要:目的查明沉默外被体蛋白复合物亚基β2(coatomer protein complex subunitβ2,COPB2)在人非小细胞肺癌细胞(A549)中的作用及其生物学机制。方法通过Western blot法检测非小细胞肺癌组织和癌旁组织、正常肺泡上皮细胞和肺癌细胞中COPB2水平。A549细胞用COPB2短发夹RNA(COPB2 shRNA)转染,MTT法测定细胞活力,EdU染色法检测细胞增殖,Transwell法检测细胞的迁移和侵袭水平,免疫印迹法检测p-AKT、AKT、Cleaved Caspase-3、cyclin D1、Bcl-2和Bax水平。结果与正常肺组织或细胞相比,非小细胞肺癌组织和细胞中COPB2水平显著上升;沉默COPB2可以显著抑制A549细胞的增殖、迁移和侵袭,降低p-AKT/AKT比值、cyclin D1和Bcl-2水平,升高Cleaved Caspase-3和Bax水平。结论沉默COPB2通过调节AKT信号通路抑制非小细胞肺癌的进展。Objective To investigate the role of silencing coatomer protein complex subunitβ2(COPB2)in human non-small cell lung cancer cells(A549)and its biological mechanism.Methods The levels of COPB2 in non-small cell lung cancer tissues and adjacent tissues,normal alveolar epithelial cells and lung cancer cells were detected by Western blotting.A549 cells were transfected with short hairpin COPB2(sh-COPB2).Cell viability was determined by MTT method,cell proliferation was detected by EdU staining method;cell migration and invasion levels were detected by Transwell method;p-AKT,AKT,cleaved caspase-3,cyclin D1,Bcl-2 and Bax proteins were detected by Western blotting.Results Compared with normal lung tissues or cells,the expression level of COPB2 in non-small cell lung cancer tissues and cells increased significantly(P<0.001);silencing COPB2 could significantly inhibit the proliferation,migration and invasion of A549 cells.The ratio of p-AKT/AKT,the protein expression levels of cyclin D1 and Bcl-2 decreased significantly,while the protein expression levels of cleaved caspase-3 and Bax increased significantly.Conclusion Silencing COPB2 inhibits the progression of non-small cell lung cancer by regulating the AKT signaling pathway.
关 键 词:非小细胞肺癌 外被体蛋白复合物亚基β2 细胞增殖 迁移 侵袭
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