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首页> 外文期刊>Cellular Signalling >Perifosine sensitizes UVB-induced apoptosis in skin cells: New implication of skin cancer prevention?
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Perifosine sensitizes UVB-induced apoptosis in skin cells: New implication of skin cancer prevention?

机译:Perifosine增强UVB诱导的皮肤细胞凋亡:预防皮肤癌的新含义?

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摘要

We demonstrate here that a relative low dose of perifosine significantly enhanced UVB-induced apoptosis in skin cells (keratinocytes and fibroblasts), associated with a significant increase of reactive oxygen species (ROS) and ceramide production as well as multiple perturbations of diverse cell signaling pathways, shifting to a significant pro-apoptosis outcomes. Perifosine inhibited UVB-induced pro-survival Akt/mammalian target of rapamycin (mTOR) and ERK activation, while facilitating pro-apoptotic AMP-activated protein kinas (AMPK), c-Jun-NH _2-kinase (JNK), and p53 activation; these signaling changes together promoted a striking increase in skin cell apoptosis and a significantly reduced amount of DNA damages. Our results suggest that perifosine may represent a novel skin cancer prevention strategy.
机译:我们在这里证明了相对较低剂量的过磷s碱显着增强了UVB诱导的皮肤细胞(角质形成细胞和成纤维细胞)凋亡,与活性氧(ROS)和神经酰胺产生的显着增加以及多种细胞信号通路的多重扰动有关,转移至明显的促凋亡结果。 Perifosine抑制UVB诱导的雷帕霉素(mTOR)和ERK激活的生存Akt /哺乳动物靶标,同时促进促凋亡的AMP激活的蛋白激酶(AMPK),c-Jun-NH _2激酶(JNK)和p53激活;这些信号改变共同促进了皮肤细胞凋亡的显着增加,并显着减少了DNA损伤的数量。我们的结果表明,periposine可能代表了一种新型的皮肤癌预防策略。

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