Oxygen-mediated endocytosis in cancer.

Oxygen-mediated endocytosis in cancer.
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DOI:
10.1111/j.1582-4934.2010.01016.x
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发表时间:
2010-03
影响因子:
5.3
通讯作者:
Ohh M
Ohh M
中科院分区:
医学2区
文献类型:
--
作者:
Wang Y;Ohh M

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实体瘤总是表现出缺氧区域和受体酪氨酸激酶(RTK)的上调,所述受体酪氨酸激酶(RTK)触发多个信号通路,包括控制细胞增殖、存活和运动性的信号通路,最终促成肿瘤发生。虽然过去的研究表明,缺氧依赖的转录和翻译诱导的几个RTK表达和各自的配体,最近的证据表明,缺氧调节RTK信号通过内吞作用,一个主要的失活途径的RTK。缺氧介导的内吞作用也被认为调节越来越多的其他膜相关蛋白如整合素和Na,K-ATP酶的活性。这些最近的发现强调了内吞作用作为一种重要的缺氧介导的调节过程在癌症中的出现。
Solid tumours invariably exhibit regions of hypoxia and up-regulation of receptor tyrosine kinases (RTKs) that trigger multiple signal pathways, including those that govern cell proliferation, survival and motility, ultimately contributing to oncogenesis. Although past studies have shown hypoxia-dependent transcriptional and translational induction of several RTK expression and their respective ligands, recent evidence suggests that hypoxia regulates RTK signalling through endocytosis, a major deactivation pathway of RTKs. Hypoxia-mediated endocytosis is also thought to modulate the activity of a growing list of other membrane-associated proteins such as integrins and Na,K-ATPase. These recent discoveries underscore the emergence of endocytosis as an important hypoxia-mediated regulatory process in cancer.
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