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首页> 外文期刊>Journal of Cellular Physiology >Hypoxia enhances cancer cell invasion through relocalization of the proprotein convertase furin from the trans-Golgi network to the cell surface.
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Hypoxia enhances cancer cell invasion through relocalization of the proprotein convertase furin from the trans-Golgi network to the cell surface.

机译：缺氧增强癌细胞的入侵relocalization proprotein的转化酶furin从trans-Golgi网络到细胞表面。

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摘要

Tumor hypoxia is strongly associated with malignant progression such as increased cell invasion and metastasis. Although the invasion-related genes affected by hypoxia have been well described, the contribution of post-transcriptional mechanisms such as protein trafficking and proprotein processing associated with the hypoxic response remains poorly understood. The proprotein convertase furin, the major processing enzyme of the secretory pathway, resides in the trans-Golgi network and most studies support a model where endogenous substrates are processed by furin within this compartment. Here, we report that hypoxia triggered an unexpected relocalization of furin from the trans-Golgi network to endosomomal compartments and the cell surface in cancer cells. Exposing these cells back to normoxic conditions reversed furin redistribution, suggesting that the tumor microenvironment modulates furin trafficking in a highly regulated manner. Assessment of the mechanisms involved revealed that both Rab4GTPase-dependent recycling and interaction of furin with the cytoskeletal anchoring protein, filamin-A, are essential for the cell surface relocalization of furin. Interference with the association of furin with filamin-A, prevented cell surface relocalization of furin and abolished the ability of cancer cells to migrate in response to hypoxia. Our observations support the notion that hypoxia promotes the formation of a peripheral processing compartment where furin translocates for enhanced processing of proproteins involved in tumorigenesis.
机译：肿瘤缺氧是密切相关的增加细胞等恶性发展入侵和转移。invasion-related基因受到缺氧的影响被描述的贡献转录后等机制的蛋白质人口贩卖和proprotein处理相关与缺氧反应仍然不佳理解。主要加工酶的分泌通路,驻留在trans-Golgi网络和最大研究支持一个内生的模型基质由furin在这个处理隔间。触发一个意想不到的relocalization furin从trans-Golgi endosomomal网络车厢,在癌症细胞表面细胞。条件逆转furin再分配,这表明肿瘤微环境调节furin贩卖一个高度管制的方式。显示两个Rab4GTPase-dependent回收与细胞骨架和交互的furin锚定蛋白,filamin-A是必不可少的细胞表面relocalization furin。干扰furin协会relocalization filamin-A,阻止细胞表面furin和废除了癌症的能力细胞迁移对缺氧的反应。观察缺氧的观念的支持促进形成一个外围处理室,furin把增强处理proproteins参与肿瘤发生。

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