人淋巴样细胞在轻度高温下通过p53依赖途径消除甲基甲磺酸诱导的微核(MNS)。

Hwa Jin Jung, Jee Na Hwang, Young R Seo
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引用次数: 0

摘要

p53介导的细胞反应在维持哺乳动物细胞抗基因毒性应激的基因组稳定性中起着至关重要的作用。在我们之前的研究中,我们发现轻度热疗足以诱导人淋巴系统p53依赖通路上的细胞凋亡(Seo et al., 1999),提示轻度热疗可能有助于减少基因组不稳定性。然而,很少有报道显示在轻度高温下p53对致癌DNA损伤的预防作用的直接证据。在这里,我们首次证明了mms诱导的微核(MN)作为致癌风险的生物标志物之一,在人淋巴样细胞对轻度高温的反应中,p53的激活消除了mms诱导的微核(MN),这强烈表明轻度高温可能在染色体稳定性中对遗传毒性应激具有保护作用。我们的数据可能支持临床应用的研究,以预防人类淋巴系统的致癌性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Elimination of methyl methanesulfonate (MMS)-induced micronuclei (MNS) under mild hyperthermia via p53-dependent pathway in human lymphoid cells.

P53-mediated cellular response has been known to play a crucial role in maintaining genomic stability of mammalian cells against genotoxic stresses. In our previous study, we showed that mild hyperthermia was sufficient to induce apoptosis on p53-dependent pathway in human lymphoid system (Seo et al., 1999), suggesting that mild hyperthermia might be useful for the reducing of genomic instability. However, there have been few reports to show the direct evidence on preventive role of p53 under mild hyperthermia against carcinogenic DNA damage. Here we first show the elimination of MMS-induced micronuclei (MN) as one of biomarkers of carcinogenic risk by p53 activation in human lymphoid cells in response to mild hyperthermia, strongly suggesting a possible protective role of mild hyperthermia in chromosomal stability against genotoxic stresses. Our data might support investigation of the clinical application of mild hyperthermia for the prevention of carcinogenesise in the human lymphoid system.

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