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首页> 外文期刊>Chemotherapy: International Journal of Experimental and Clinical Chemotherapy >Bcl-xL Antisense Oligonucleotides Chemosensitize Human Glioblastoma Cells.
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Bcl-xL Antisense Oligonucleotides Chemosensitize Human Glioblastoma Cells.

机译：Bcl-xL反义寡核苷酸对人胶质母细胞瘤细胞具有化学敏感性。

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Background: Resistance to chemotherapy in glioblastoma has been linked to the expression of antiapoptotic Bcl-2 family members including Bcl-xL. Methods: Bcl-xL expression was specifically reduced in M059K glioblastoma cells with antisense oligonucleotides (ISIS 16009, ISIS 16967) as assessed by Western blotting. Induction of apoptosis by treatment with antisense oligonucleotides in combination with paclitaxel in cell culture was monitored by WST-1 assays and flow cytometric analysis. Results: Antisense oligonucleotide-mediated reduction of Bcl-xL levels led to enhanced cytotoxicity in M059K cells when compared to the use of a mismatch control oligonucleotide (p < 0.001). A decreased threshold for the induction of apoptosis led to significantly enhanced cytotoxic responses to paclitaxel treatment in WST-1 assays (p < 0.001) and flow cytometric analyses. Conclusion: Combination treatment using Bcl-xL antisense oligonucleotides and paclitaxel may qualify as a promising strategy to ultimately improve the clinical outcome of glioblastoma.
机译：背景：胶质母细胞瘤对化学疗法的耐药性已与抗凋亡Bcl-2家族成员（包括Bcl-xL）的表达有关。方法：通过Western印迹评估，在具有反义寡核苷酸（ISIS 16009，ISIS 16967）的M059K胶质母细胞瘤细胞中Bcl-xL表达被特异性降低。通过WST-1测定法和流式细胞术分析监测通过反义寡核苷酸与紫杉醇结合在细胞培养物中处理引起的细胞凋亡。结果：与使用错配对照寡核苷酸相比，反义寡核苷酸介导的Bcl-xL水平降低导致M059K细胞的细胞毒性增强（p <0.001）。在WST-1分析（p <0.001）和流式细胞仪分析中，诱导凋亡的阈值降低导致对紫杉醇治疗的细胞毒性反应显着增强（p <0.001）。结论：使用Bcl-xL反义寡核苷酸和紫杉醇的联合治疗可能成为最终改善胶质母细胞瘤临床结果的有希望的策略。

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