逆癌酮诱导人肺癌细胞凋亡的体外研究

External Study on Apoptosis of Human Lung Cencer Cells Induced by Anticancer Ketonon

目的:研究逆癌酮诱导A549人肺腺癌细胞系和PLA-801D人肺巨细胞癌细胞系凋亡及其抗癌作用机理。方法:应用体外细胞培养技术,以逆癌酮作用于肺癌细胞,绘制生长曲线,作克隆形成实验,观察其对细胞增殖的影响,并进行光镜和流式细胞术的观察和分析。结果:应用逆癌酮后细胞生长明显受抑,克隆形成能力降低,流式细胞分析表明,应用逆癌酮后,肺癌细胞凋亡指数显著增加(P<0.01),细胞被阻滞于G0/G1期(P<0.01),其bax、Fas的表达被上调;bcl-2的表达被下调(P<0.01);c-myc、TGFβR1的表达也被上调(P<0.01)。结论:逆癌酮对A549细胞和PLA-801D细胞有明显的细胞毒熏并通过上调bax、Fas的表达,下调bcl-2的表达诱导细胞凋亡。

Objective: The apoptosis of A549human lung adecarcinoma cell line and PLA)801D h uman lung giant cell cancer cell line induced by anticancer ketonon was studied in order to explore its mechanism of antineoplastic effect. Methods: By techniques of cell culture in vitro,lung cancer cells were treated by an ticancer ketonon.Then observed and analysed by growth)curves,clone experiment and light microscopy.The expression of apoptosis)related gene was detected by flow cytometry. Re)sults: The proliferation of A549cells and PLA)801D cells was inhibited evide ntly after treatment by anticancer ketonon.Ability of clone formation was also inhibited.Apoptosis index was enhanced and cells were blocked at G 0/G 1 phrase(P<0.01).Bax and Fas expression was up)regulated(P<0.01 )and Bcl)2expression was down)regulated(P<0.01).c)myc?TGF a R1expression was up)regulated(P<0.01). Conclusion: Anticancer ketonon has remarkable cytotoxity and could induce the apoptosis of A549cells and PLA)801D cells by up)regulating expression of Bax and F as and down)regulating expression of Bcl)2.