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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Olaparib Potentiates Anticancer Drug Cytotoxicity via 53BP1 in Oesophageal Squamous Cell Carcinoma Cells
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Olaparib Potentiates Anticancer Drug Cytotoxicity via 53BP1 in Oesophageal Squamous Cell Carcinoma Cells

机译：Olaparib通过53bp1在食管鳞状细胞癌细胞中引起抗癌药物细胞毒性

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摘要

Background/Aim: Olaparib was previously shown to synergistically enhance the cytotoxicity of DNA synthesis inhibitors in oesophageal carcinoma (OC) cell lines. However, the mechanisms of this synergy are not fully understood. As P53 binding protein 1 (53BP1) expression was previously shown to potentiate the anticancer effect of olaparib, we investigated the involvement of 53BP1 in the synergetic cytotoxic effects of olaparib and anticancer drugs in KYSE70 cells. Materials and Methods: Experiments included small interfering RNA transfection, growth inhibition assays, western blots, immunofluorescence, and flow cytometry. Results: The toxicity of DNA synthesis-inhibiting agents plus olaparib was decreased when 53BP1 was depleted. Olaparib cotreatment significantly increased phosphorylated H2A histone family member X (gamma H2AX) foci as well as 53BP1/gamma H2AX co-localisation in anticancer drug-treated cells. Silencing of 53BP1 suppressed anticancer drug-induced apoptosis with or without olaparib. Conclusion: Olaparib potentiates the cytotoxicity of anticancer drugs through 53BP1 in OC cells.
机译：背景/目的：奥拉帕里布预先证明了在食管癌（OC）细胞系中的DNA合成抑制剂的细胞毒性。但是，这种协同作用的机制尚不完全明白。作为P53结合蛋白1（53bp1）表达先前显示出奥拉帕里布的抗癌作用，我们研究了53bp1在Kyse70细胞中奥拉帕里布和抗癌药物的协同细胞毒性作用。材料和方法：实验包括小干扰RNA转染，生长抑制测定，蛋白质印迹，免疫荧光和流式细胞术。结果：当53bp1耗尽时，DNA合成抑制剂加olaparib的毒性降低。奥拉帕里布加治疗显着增加了磷酸化的H2A组蛋白家族构件X（Gamma H2AX）焦点以及抗癌药物处理细胞的53bp1 / gamma h2ax共定位。 53bp1的沉默抑制了抗癌药物诱导的细胞凋亡，或没有olaparib。结论：奥拉帕里布通过53bp1在OC细胞中加强了抗癌药物的细胞毒性。

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