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首页> 外文期刊>Journal of Cellular Physiology >p53-Mediated enhancement of radiosensitivity by selenophosphate synthetase 1 overexpression.
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p53-Mediated enhancement of radiosensitivity by selenophosphate synthetase 1 overexpression.

机译：p53-Mediated增强辐射敏感度的selenophosphate合成酶1超表达。

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摘要

Selenium has been associated with cancer prevention. Despite vast knowledge of selenium effect on various health conditions, functional characterization of selenium metabolic enzymes on cellular physiology has been limited. Therefore, to gain insight into the mechanisms underlying cancer prevention by selenium, we investigated sps1, one of the two human selenophosphate synthetase genes for its role in cancer cell's response to ionizing radiation. Although stable expression of Sps1 protein per se had little effect on cell proliferation, concurrent irradiation decreased viability of the sps1 cell line. The increased sensitivity of the cell lines to ionizing radiation was correlated with increased p53 activity as well as with simultaneous up- and downregulation of Bax and Bcl2, respectively. Knockdown of sps1 and p53 by small interfering RNA method revealed that the level of p53 was proportional to that of Sps1 and that the increased radiosensitivity was dependent upon p53. Sps1 cell lines displayed decreased level of reactive oxygen species (ROS) with concomitant increase of certain redox enzymes. Furthermore, p53 activity was regulated by cellular redox via Ref1 in sps1 cell lines. Collectively, our results demonstrated that sps1 was able to affect cell viability upon ionizing radiation via modulation of p53 activity. They further suggest that Sps1 and its reaction product selenophosphate might be involved in cancer prevention in a p53-dependent manner and could be applied to development of a novel cancer therapy.
机译：硒与癌症有关预防。影响不同的健康状况,功能硒代谢酶的特性细胞生理学是有限的。洞察机制硒预防癌症,我们调查sps1,两个人类selenophosphate之一合成酶基因在癌细胞的作用对电离辐射的反应。表达Sps1蛋白质本身几乎没有对细胞增殖的影响,并发辐照sps1细胞的生存能力下降线。电离辐射与p53活动以及增加同时伯灵顿和差别,对这些基因分别Bcl2。小干扰RNA方法显示水平的p53 Sps1和成正比增加辐射敏感度是相关的p53。活性氧(ROS)伴随增加某些氧化还原酶。此外,p53活动受通过在sps1 Ref1细胞系细胞氧化还原。总的来说,我们的研究结果表明,sps1能够影响细胞的生存能力在电离通过调制辐射p53的活动。进一步表明Sps1和其反应产品selenophosphate可能参与癌症预防p53-dependent的方式可以应用于小说的发展癌症吗治疗。

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