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| 低剂量拓扑替康诱导肺癌脑转移HTB-56／DDP细胞株凋亡机制的研究 | |
| 引用本文： | 高文斌,郑真真,高丰,韩传军,黄建辉,张晓晨,王武龙,汪艾曼,王若雨,方今女. 低剂量拓扑替康诱导肺癌脑转移HTB-56／DDP细胞株凋亡机制的研究[J]. 中华肺部疾病杂志(电子版), 2012, 0(5): 440-444 |
| 作者姓名： | 高文斌 郑真真 高丰 韩传军 黄建辉 张晓晨 王武龙 汪艾曼 王若雨 方今女 |
| 作者单位： | 大连大学附属中山医院肿瘤科;大连大学研究生院;包头医学院第二附属医院放疗科;包头医学院第三附属医院仪检中心;延边大学医学部病理及病理生理学教研室 |
| 基金项目： | 2009年大连市科技局科技计划项目(2009E11SF231) |
| 摘 要： | 目的探讨低剂量拓扑替康（TPT）治疗肺癌脑转移的机制。方法采用体外培养耐顺铂肺腺癌细胞HTB-56／DDP，并用Annexin V-FITC染色法检测细胞的早期凋亡；PI单染色法检测细胞周期。结果Caspase-3、8特异性抑制剂和TPT联用组与单用TPT组相比其存活率较高（P〈0．05）；TPT组（6．4μmol·L-1）于12h出现早期凋亡，caspase抑制剂组出现延迟，凋亡率降低；流式细胞仪检测到细胞周期发生改变，G1期细胞较对照组增多（P〈0．05），S期细胞减少（P〈0．05）。结论低剂量TPT治疗肺癌脑转移的机制可能与其诱导肿瘤细胞凋亡相关，该过程与caspase-3、8的相关活化过程有关。 |
| 关 键 词： | 肺癌 脑转移 拓扑替康 凋亡 半胱天冬酶 |
Study about the mechanism of low dose topotecan on lung cancer cell lines HTB-56/DDP with brain metastasis |
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| Affiliation: | GAO Wen-bin1,ZHENG Zhen-zhen2,GAO Feng2,HAN Chuan-jun2,HUANG Jian-hui2,ZHANG Xiao-chen2,WANG Wu-long23,WANG Ai-man4,WANG Ruo-yü1,FANG Jin-nü5(1Oncology Department,Zhongshan Hospital Affiliated to Dalian University,Dalian,116001,China;2Graduate School,Dalian University,Dalian,116001,China;3Radiotherapy Department;4Instrumental Testing Centre,The Second Affiliated Hospital of Baotou Medical college,Baotou,014030,China;5Pathology and Pathophysiology Teaching and Research Office,Yanbian University of Medicine,Yanbian,133000 China) |
| Abstract: | Objective To study about the mechanism of topotecan （TPT） on lung cancer with brain metastasis. Methods Incubating anti-cisplatin pulmonary adenocarcinoma cells HTB- 56/DDP to a certain time. The inhibition rate of HTB-56/DDP was measured by MTT assay, The early apoptosis was detected by Annexin V-FITC . The changes of cell cycle was detected by PI single stain. Result The survival ratios of caspase-3, 8 specific inhibitor group was higher than the TPT single group. TPT group（6.4μmol·L-1 ） appeared early apoptosis at 12 h, while it did not happened in the group with caspase specific inhibitor. The cell cycle was detected by flow cytometry. G1 stage significant was more than control group（P 〈0.05 ） and S stage significant was less cytometer（FCM） than control group（ P 〈 0.05 ）. Conclusion The mechanism of TPT on lung cancer with brain metastasis can be induced the apoptosis and this process involved the activation of caspase-3,8. |
| Keywords: | Lung carcinoma Brain metastasis Toptecan Apoptosis Caspase |
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