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Radiosensitization of esophageal cancer cells ECA109 by knockdown of H2AX

机译：敲除H2AX对食管癌细胞ECA109的放射增敏作用

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Background: Genetic studies on mice have demonstrated that the key regulator of DNA damage in mammalian cells is the histone H2A variant, H2AX. We hypothesize that knockdown of H2AX will cause DNA damage pathway defects and may be able to increase the sensitivity to radiotherapy. Methods: The formation of foci and the interaction of several important proteins in esophageal cancer ECA109, triggered by irradiation, were detected by immunofluorescence staining and Co-immunoprecipitation (Co-IP) assay before and after H2AX silencing. Clone formation assay was employed to detect cell radiosensitivity and cloning formation ability also before and after H2AX silencing. Cell cycle distribution and apoptosis were detected by flow cytometry. We constructed a nude mice esophageal cancer model and detected the above contents in vivo. Results: H2AX and several proteins could form foci in nuclear triggered by irradiation and establish a relationship in vitro. The foci reduced after H2AX silencing. H2AX silencing could lead to radiosensitization via a colony-forming test. The apoptosis rate increased and the cell cycle was blocked in G2-M stage after H2AX silencing in vivo. The tumor volume was decreased in the H2AX silenced group after irradiation, while the tumor only slowed down the growth rate in the control groups. Conclusions: Knockdown of H2AX induced radiosensitization of esophageal cancer ECA109 cells both in vitro and in vivo. The mechanisms include defective cell cycle checkpoints and abolishment of foci formation for several important mediator and effector proteins in the DNA damage response to irradiation (IR).
机译：背景：对小鼠的遗传研究表明，哺乳动物细胞中DNA损伤的关键调节因子是组蛋白H2A变体H2AX。我们假设敲低H2AX会导致DNA损伤途径缺陷，并可能增加对放射疗法的敏感性。方法：采用免疫荧光染色和免疫共沉淀（Co-IP）法检测H2AX沉默前后食管癌ECA109中病灶的形成和几种重要蛋白的相互作用。在H2AX沉默之前和之后，都使用克隆形成测定来检测细胞的放射敏感性和克隆形成能力。流式细胞仪检测细胞周期分布和凋亡。我们构建了一个裸鼠食道癌模型，并在体内检测到上述含量。结果：H2AX和几种蛋白质可在辐射触发下在核内形成灶，并在体外建立关系。 H2AX沉默后，病灶减少。 H2AX沉默可能会通过菌落形成测试导致放射增敏。体内H2AX沉默后，在G2-M期细胞凋亡率增加，细胞周期受阻。 H2AX沉默组在照射后肿瘤体积减小，而对照组中肿瘤仅减慢了生长速度。结论：敲除H2AX可以在体内和体外诱导食管癌ECA109细胞的放射增敏作用。该机制包括有缺陷的细胞周期检查点和废除DNA对辐射（IR）的损伤反应中几种重要介体和效应蛋白的形成灶。

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