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首页> 外文期刊>Molecular and Cellular Biology >Regulation of c-jun expression during hypoxic and low-glucose stress.
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Regulation of c-jun expression during hypoxic and low-glucose stress.

机译：低氧和低糖应激时c-jun表达的调节。

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Hypoxic stress in tumor cells has been implicated in malignant progression and in the development of therapeutic resistance. We have investigated the effects of acute hypoxic exposure on regulation of the proto-oncogene c-jun in SiHa cells, a human squamous carcinoma cell line. Hypoxic exposure produced increased levels of c-jun mRNA resulting from both message stabilization and transcriptional activation. A superinduction of c-jun message resulted during simultaneous oxygen and glucose deprivation, with several characteristics of an induction mediated by oxidative-stress pathways. This superinduction was blocked by preincubation of cells with the glutathione precursor N-acetyl cysteine or with phorbol 12-myristate 13-acetate, which indicates redox control of c-jun expression and probable involvement of protein kinase C. By gel retardation assay, no increase in AP-1 DNA binding activity was found to be concomitant with the transcriptional activation of c-jun. A lack of increased DNA binding was observed for the consensus AP-1 sequence and for the two AP-1 sequence variants found within the c-Jun promoter. Additionally, hypoxic and low-glucose stress produced no activation of stably transfected AP-1 reporter sequences. Taken together, these results indicate that the transcriptional activation of c-jun during hypoxic and low-glucose stress involves redox control and is unlikely to be mediated by AP-1 recognition elements within the c-jun promoter.
机译：肿瘤细胞中的低氧应激与恶性进展和治疗抗性的发展有关。我们研究了急性缺氧暴露对人鳞状细胞癌细胞系SiHa细胞中原癌基因c-jun调控的影响。缺氧暴露导致c-jun mRNA水平升高，这是由于消息稳定和转录激活所致。 c-jun信息的超诱导导致同时缺氧和缺糖，具有氧化应激途径介导的诱导的几个特征。通过与谷胱甘肽前体N-乙酰半胱氨酸或佛波醇12-肉豆蔻酸酯13-乙酸酯预孵育细胞来阻止这种超诱导，这表明c-jun表达的氧化还原控制和蛋白激酶C的可能参与。通过凝胶阻滞测定，没有增加在AP-1中发现DNA结合活性与c-jun的转录激活相伴。对于共有的AP-1序列和在c-Jun启动子中发现的两个AP-1序列变体，观察到缺乏增加的DNA结合。另外，低氧和低葡萄糖应激不会产生稳定转染的AP-1报告基因序列的激活。综上所述，这些结果表明在低氧和低葡萄糖应激期间c-jun的转录激活涉及氧化还原控制，并且不太可能由c-jun启动子内的AP-1识别元件介导。

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