CAJ | 학술논문

目的观察抑癌基因SARI在雌激素诱导的肺腺癌细胞增殖中的作用及其相关分子信号通路.方法通过质粒转染的方法在肺腺癌细胞A549中过表达SARI蛋白,噻唑蓝(MTT)比色法观察雌激素处理前后细胞的增殖,Western blot法检测雌激素诱导的细胞增殖信号通路中相关蛋白肉瘤病毒基因(Src)、蛋白激酶B(Akt)及细胞外调节蛋白激酶(Erk)的表达及活化.结果 MTT实验结果显示,过表达SARI显著抑制雌激素诱导的A549细胞增殖,A549细胞增殖率下降56％ (P ＜0.05);Western blot实验结果显示,过表达SARI的A549细胞在雌激素处理后,其磷酸化肉瘤病毒基因(pSrcy416)、磷酸化蛋白激酶B(pAkts473)及磷酸化细胞外调节蛋白激酶(pErk)表达显著下调(P＜0.05),而Src、Akt及Erk蛋白表达不变.结论 SARI能够抑制雌激素诱导的肺腺癌细胞增殖,潜在的机制可能是通过抑制肺腺癌细胞中Src-Akt-Erk信号通路活化.
목적 관찰억암기인SARI재자격소유도적폐선암세포증식중적작용급기상관분자신호통로.방법 통과질립전염적방법재폐선암세포A549중과표체SARI단백,새서람(MTT)비색법관찰자격소처리전후세포적증식,Western blot법검측자격소유도적세포증식신호통로중상관단백육류병독기인(Src)、단백격매B(Akt)급세포외조절단백격매(Erk)적표체급활화.결과 MTT실험결과현시,과표체SARI현저억제자격소유도적A549세포증식,A549세포증식솔하강56％ (P ＜0.05);Western blot실험결과현시,과표체SARI적A549세포재자격소처리후,기린산화육류병독기인(pSrcy416)、린산화단백격매B(pAkts473)급린산화세포외조절단백격매(pErk)표체현저하조(P＜0.05),이Src、Akt급Erk단백표체불변.결론 SARI능구억제자격소유도적폐선암세포증식,잠재적궤제가능시통과억제폐선암세포중Src-Akt-Erk신호통로활화.
Objective To investigate the function of tumor suppressor gene suppressor of activator protein-1 (AP-1),regulated by interferon (IFN) in Estradiol-induced cell proliferation of lung adenocarcinoma and its underlying signal pathways.Methods We transfected pcDNA-SARI in A549 cells to overexpress SARI.3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to detect cell proliferation.Western blotting was used to analyze the protein levels of sarcoma gene (Src),extracellular regulated protein kinases (Erk2),protein kinase B (Akt) and phosphorylated sarcoma gene (pSrcy416),phosphorylated protein kinase B (pErk),phosphorylated extracellular regulated protein kinases (pAkta473).Results MTT assay showed overexpression of SARI significantly inhibited cell proliferation induced by estradiol in A549 cell lines,proliferation rate was decreased by 56％ (P ＜ 0.05) ; Western blotting assay indicated the protein levels of pSrcy416,pAkta473 and pErk decreased in SARI overexpression A549 cells after estradiol treatment (P ＜ 0.05),while protein levels of Src,Akt and Erk2 kept unchanged.Conclusion SARI inhibited Estradiol-induced cell proliferation of lung adenocarcinoma.The underlying mechauisms were likely to attenuating the Src-Akt-Erk signal pathways.