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作 者:王道威[1] 刘俊[1] 张彬[1] 张华[1] 高留伟 王长利[1]
机构地区:[1]天津医科大学肿瘤医院肺部肿瘤科国家肿瘤临床医学研究中心天津市肿瘤防治重点实验室天津市肺癌诊治中心,300060
出 处:《中华实验外科杂志》2014年第11期2473-2475,共3页Chinese Journal of Experimental Surgery
基 金:天津市科委应用基础面上资助项目(12JCYBJC17800);天津市科委抗癌重大专项(12ZCDZSY15400)
摘 要: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.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 (pSrc^y416),phosphorylated protein kinase B (pErk),phosphorylated extracellular regulated protein kinases (pAkt^s473).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 pSrc^y416,pAkt^s473 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.
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