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生长因子信号允许缺氧诱导的自噬通过人类癌细胞中 HIF1alpha 依赖性、BNIP3/3L 非依赖性转录程序。

Growth factor signaling permits hypoxia-induced autophagy by a HIF1alpha-dependent, BNIP3/3L-independent transcriptional program in human cancer cells.

机构信息

Tumour Cell Death Laboratory, Beatson Institute for Cancer Research, Glasgow, UK.

出版信息

Autophagy. 2009 Oct;5(7):1068-9. doi: 10.4161/auto.5.7.9821. Epub 2009 Oct 13.

DOI:10.4161/auto.5.7.9821
PMID:19738440
Abstract

Several recent reports have demonstrated that autophagy is induced in response to hypoxia in cultured cells. However, the mechanism and consequence of hypoxia-induced autophagy remains unclear as there is no consensus between these studies. In our recent report we show that, in human cancer cells, hypoxia cooperates with growth factor signaling to facilitate a HIF1alpha-driven transcriptional response that promotes autophagy. Here we summarize these findings and set them in context of the findings of other groups, concluding that there are likely multiple routes to different forms of autophagy that serve different purposes downstream of hypoxia, depending upon the degree of stress and cellular context.

摘要

最近有几项报告表明,自噬是在培养细胞缺氧时被诱导的。然而,由于这些研究之间没有共识,因此缺氧诱导自噬的机制和后果仍不清楚。在我们最近的报告中,我们表明在人类癌细胞中,缺氧与生长因子信号协同作用,促进 HIF1alpha 驱动的转录反应,从而促进自噬。在这里,我们总结了这些发现,并将其置于其他研究小组的发现背景下,得出的结论是,可能存在多种途径导致不同形式的自噬,这些自噬在下游缺氧时具有不同的功能,具体取决于应激程度和细胞环境。

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Opportunities and challenges of co-targeting epidermal growth factor receptor and autophagy signaling in non-small cell lung cancer.非小细胞肺癌中同时靶向表皮生长因子受体和自噬信号传导的机遇与挑战
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The incredible ULKs.不可思议的 ULKs。
Cell Commun Signal. 2012 Mar 13;10(1):7. doi: 10.1186/1478-811X-10-7.
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