| 吉非替尼对非小细胞肺癌细胞的体外抑制作用 |
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| 引用本文： | 陈真,李子明,陈智伟. 吉非替尼对非小细胞肺癌细胞的体外抑制作用[J]. 肿瘤研究与临床, 2011, 23(6): 393-395. DOI: 10.3760/cma.j.issn.1006-9801.2011.06.010 |
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| 作者姓名： | 陈真 李子明 陈智伟 |
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| 作者单位： | 1. 上海市杨浦区市东医院病理科,200438
2. 上海交通大学附属胸科医院,上海市肺部肿瘤临床医学中心 |
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| 摘 要： | 目的研究体外吉非替尼对非小细胞肺癌细胞株的作用机制。方法观察吉非替尼作用于A549、SPC-A-1、H460、H1229、95D5株人类非小细胞肺癌细胞株，应用活细胞计数试剂盒CCK8测定各组细胞增殖抑制情况；选择A549、SPC-A-1细胞株，PI标记后应用流式细胞术观察细胞凋亡状况，Transweu方法检测细胞侵袭情况；Westernblot检测药物对增殖相关信号通路蛋白表达的变化。结果吉非替尼抑制了各株肺癌细胞的增殖和侵袭（P〈0．05）；吉非替尼组中A549和SPC-A-1细胞的凋亡率分别为（9．6±0．73）％和（14．3±1．12）％，高于对照组的（3．1±0．29）％（t=11．16，P=0．001；t－4．726，P=0．009）；吉非替尼作用于A549细胞72h后，能明显降低p-AKT、P—EGFR、p-MAPK蛋白的表达水平（t=6．656，P=0．003；t=16．441，P=0．0001；t=3．736，P=0．020）。结论吉非替尼能抑制肺癌细胞在体外的增殖、侵袭，可诱导肿瘤细胞的凋亡，其作用可能与下调活化的表皮生长因子受体（EGFR）信号转导通路关键酶的表达有关。
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| 关 键 词： | 肺肿瘤 吉非替尼 细胞增殖 细胞凋亡 受体 血管内皮生长因子 |
Inhibition effects of gefitinib on non-small cell lung cancer cell lines in vitro |
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| CHEN Zhen,LI Zi-ming,CHEN Zhi-wei. Inhibition effects of gefitinib on non-small cell lung cancer cell lines in vitro[J]. Cancer Research and Clinic, 2011, 23(6): 393-395. DOI: 10.3760/cma.j.issn.1006-9801.2011.06.010 |
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| Authors: | CHEN Zhen LI Zi-ming CHEN Zhi-wei |
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| Affiliation: | . Department of Pathology, Shidong Hospital in Yangpu District, Shanghai 200438, China |
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| Abstract: | Objective To explore the mechanism of gefitinib in the treatment of non-small cell lung cancer (NSCLC) cell lines in vitro. Methods The effects of the gefitinib in five human NSCLC cell lines (A549, SPC-A-1, H460, H1229, 95D) were studied. The inhibition of cell proliferation in each group were measured by CCK8;The status of apoptosis cells were observed using flow cytometry after PI marked;invasion of lung cancer cell inhibited by gefitinib were assessed by transwell technique;The drug was detected by western blot on the proliferation-related signaling protein. Results The proliferation and invasive capacity of NSCLC cells were inhibited by gefitinib (P < 0.05). In gefitinib group, the apoptosis rates of A549 [(9.6±0.73) %]and SPC-A-1[(14.3±1.12) %]were higher than that of control group[(3.1±0.29) %](t =11.16,P =0.001;t =4.726, P =0.009). Expression of p-AKT, p-EGFR, p-MAPK protein levels were significantly down regulated in A549 cells when gefitinib was given after 72 hours (t =6.656, P =0.003;t =16.441, P =0.0001;t =3.736, P =0.020). Conclusion Gefitinib can inhibit the proliferation and invasion of lung cancer cell, also can induce apoptosis in vitro and most likely to contribute to the inhibition of key enzymes in EGFR signaling transduction pathway. |
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| Keywords: | Lung neoplasms Gefitinib Cell proliferation Apoptosis Receptere,vascular endothelial growth factor |
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