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细胞自噬对紫杉醇诱导人卵巢癌细胞HO-8910凋亡的影响 被引量：3

Effect of autophagy on paclitaxel-induced apoptosis of human ovarian cancer cell HO-8910
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摘要 目的探讨紫杉醇体外对人卵巢癌细胞株HO-8910自噬的影响。方法体外培养人卵巢癌细胞HO-8910。不同浓度紫杉醇作用24、48、72h后,采用MTT比色法检测细胞增殖,流式细胞术检测细胞自噬小体含量,Western blot测定自噬相关蛋白Beclin-1和LC3的表达水平,并检测Akt、磷酸化Akt(p-Akt)和磷脂酰肌醇3-激酶(PI3K)的表达变化。结果紫杉醇可诱导HO-8910细胞发生凋亡,同时存在其他类型的死亡。紫杉醇0.1μmol/L作用24h,Beclin-1和LC3蛋白的表达水平均升高,p-Akt和PI3K的蛋白水平明显降低。结论紫杉醇可诱导体外对人卵巢癌细胞株HO-8910发生自噬。其作用机制可能与上调自噬相关基因表达和抑制自噬负调控PI3K-Akt信号转导通路有关。 Objective To study the effect of paclitaxel on autophagy of human ovarian cancer cell HO-8910. Methods The HO-8910 ceils were cultured and treated with paclitaxel in different concentrations for 24,48 and 72 hours. The cell apoptosis rates and cell death rates were determined by flow cytometry and MTT colorimetry, respectively. Autophagy and autoghagic cell death were detected using flow cytometry. With Western blot assay, the expressions of autophagic relative protein LC3 and Beclin 1,Akt and PI3K proteins were detected. Results Paclitaxel induced the apoptosis of HO-8910 cells and other kinds of non apoptosis cell death. The expressions of LC3 and Beclin 1 were increased and those of p-Akt and PI3K were decreased in HO-8910 cells after treated with paclitaxel 0. 1 tanol/L for 24 hours. Conclusion Paclitaxel can induce autophagy and autophagic cell death in HO-8910 cells, which may he related to the upregulation of some autophage-related genes expressions and downregulation of PI3K Akt signaling pathway.
作者 武玉 严沁 卢春 冷水龙 戴辉华 贾雪梅
机构地区 南京医科大学第一附属医院妇科 南京医科大学微生物与免疫学系 广州医学院解剖学系
出处 《江苏医药》 CAS 北大核心 2014年第6期630-633,共4页 Jiangsu Medical Journal
基金 江苏省六大人才高峰资助项目(WSW-124-085)
关键词 紫杉醇 卵巢癌 细胞自噬HO-8910 Paclitaxel Ovarian cancer Cell auophagy HO-8910
分类号 R737 [医药卫生—肿瘤]
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同被引文献26

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江苏医药
2014年 第6期

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