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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >ADP-ribosylation factor 6 regulates tumor cell invasion through the activation of the MEK/ERK signaling pathway.
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ADP-ribosylation factor 6 regulates tumor cell invasion through the activation of the MEK/ERK signaling pathway.

机译：ADP-核糖基化因子6通过激活MEK / ERK信号通路调节肿瘤细胞的侵袭。

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摘要

Tumor cell invasion through the extracellular matrix is accompanied by the formation of invadopodia, which are actin-rich protrusions at the adherent surface of cells at sites of extracellular matrix degradation. Using the invasive human melanoma cell line LOX as a model system, we demonstrate that the ADP-ribosylation factor 6 (ARF6) GTPase is an important regulator of invadopodia formation and cell invasion. We show that ARF6 localizes to invadopodia of LOX cells. Sustained activation of ARF6 significantly enhances the invasive capacity of melanoma as well as breast tumor cell lines, whereas dominant negative ARF6 abolishes basal cell invasive capacity as well as invasion induced by growth factors. Furthermore, using biochemical assays, we show that enhanced invasive capacity is accompanied by the activation of endogenous ARF6. Finally, we provide evidence that ARF6-enhanced melanoma cell invasion depends on the activation of the extracellular signal-regulated kinase (ERK), and that the ARF6 GTPase cycle regulates ERK activation. This study describes a vital role for ARF6 in melanoma cell invasion and documents a link between ARF6-mediated signaling and ERK activation.
机译：肿瘤细胞通过细胞外基质的侵袭伴随着侵袭足的形成，侵袭足是细胞外基质降解部位细胞粘附表面富含肌动蛋白的突起。使用侵袭性人类黑素瘤细胞系LOX作为模型系统，我们证明ADP-核糖基化因子6（ARF6）GTPase是侵袭性伪足形成和细胞侵袭的重要调节剂。我们显示ARF6本地化LOX细胞的侵袭。持续激活ARF6可以显着增强黑色素瘤以及乳腺肿瘤细胞系的侵袭能力，而显性阴性ARF6则可以消除基础细胞的侵袭能力以及由生长因子引起的侵袭。此外，使用生化分析，我们显示增强的侵袭能力伴随着内源性ARF6的激活。最后，我们提供证据表明ARF6增强的黑色素瘤细胞侵袭取决于细胞外信号调节激酶（ERK）的激活，并且ARF6 GTPase循环调节ERK激活。这项研究描述了ARF6在黑色素瘤细胞侵袭中的重要作用，并记录了ARF6介导的信号传导与ERK激活之间的联系。

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