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首页> 外文期刊>Cell cycle >The dark side of fly TNF: an ancient developmental proof reading mechanism turned into tumor promoter.
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The dark side of fly TNF: an ancient developmental proof reading mechanism turned into tumor promoter.

机译：果蝇TNF的阴暗面：一种古老的发展证明阅读机制变成了肿瘤启动子。

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摘要

The fruit fly Drosophila is an important model for biological research; however, due to its relatively short lifespan its relevance in cancer research is often questioned. Nevertheless, among many other intriguing Drosophila models, scribble group mutants provided early evidence for the existence of tumor suppressor genes and their importance in mammalian systems is beginning to emerge. In this review, I discuss recent advances in our understanding of the phenotypes of scrib group mutants, in which the activation of JNK signaling plays a crucial role. Several mechanisms can account for the activation of JNK within scrib group mutant cells, including a mechanical stress triggered by the loss of polarity, cell competition, intrinsic tumor suppression by autonomous production of Eiger, and an inflammatory response mediated by Eiger-producing haemocytes. Eiger, the sole Drosophila homolog of tumor necrosis factor, is emerging as a 'danger signal' initiated upon the presence of external pathogens, damaged tissues and the appearance of pre-malignant cells. Remarkably, in the presence of the Ras oncoprotein Eiger can act as a tumor promoter by stimulating invasive migration and delaying the onset of metamorphosis.
机译：果蝇果蝇是生物学研究的重要模型。然而，由于其相对较短的寿命，其在癌症研究中的相关性经常受到质疑。然而，在许多其他有趣的果蝇模型中，自由组合突变体为肿瘤抑制基因的存在提供了早期证据，并且它们在哺乳动物系统中的重要性开始显现。在这篇综述中，我讨论了scrib组突变体表型理解的最新进展，其中JNK信号的激活起着至关重要的作用。几种机制可以解释scrib组突变细胞内JNK的激活，包括由极性丧失触发的机械应激，细胞竞争，通过自主产生Eiger抑制内在的肿瘤以及由产生Eiger的血细胞介导的炎症反应。艾格峰（Eiger）是肿瘤坏死因子的唯一果蝇同源物，它是由于外部病原体，受损组织和恶性前细胞的出现而引发的“危险信号”。值得注意的是，在存在Ras癌蛋白的情况下，Eiger可以通过刺激侵袭性迁移和延迟变态的发生而充当肿瘤启动子。

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