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机构地区:[1]中国医学大学附属第一医院胸外科
出 处:《中国肿瘤临床与康复》1999年第2期6-8,共3页Chinese Journal of Clinical Oncology and Rehabilitation
摘 要:目的探讨VP-16对肺腺癌细胞凋亡的诱导作用。方法采用光镜、电镜、流式细胞仪、凝胶电泳和TdT原位末端标记法检测VP-16诱导人肺腺癌AGZY-83-α细胞凋亡规律,并观察放线菌酮对凋亡的抑制程度。结果VP-16在显著抑制细胞增殖的同时,能够诱导细胞凋亡,将细胞阻滞于G2期。放线菌酮对凋亡有显著的抑制作用。结论VP-16诱导细胞凋亡,是其杀死肿瘤细胞的重要机制之一。该凋亡具有明显的时间和剂量依赖性。Objectives To shed light upon the induction of apoptosis by Etoposide (VP-16) in lung cancer cells. Methods With the use of fluorescence microscopy, electron microscopy, flow cytometry,DNA gel electrophoresis and TdT-mediated dUTP-biotin nick end labelling (TUNEL), induction of apoptosis by VP-16 was investigated and the inhibition of DNA fragmentation by l g/ml cycloheximide was examined on 1.5% agarose gel electrophoresis. WTHZResults VP-16 not only caused significant growth inhibition, but also induced extensive apoptosis. When examined by light microscopy and electron microscopy, the dead cells showed morphological characteristics of apoptosis. DNA fragmentation was detected on electrophoresis and was markedly suppressed by cycloheximide, indicating that cycloheximide provided protection from VP-16 induced cytotoxicity. DNA histogram of flow cytometry showed increased apoptotic peak (Ap peak), and cells were arrested in G2 phase. ConclusionZThe induction of apoptosis by VP-16 may play a key role in its antineoplastic effect. The mode of cell death is dependent on the concentration of the agent used and the time of cell exposure.
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