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过度磷酸化的 FAK 从黏着斑转移到膜皱褶。

Hyperphosphorylated FAK Delocalizes from Focal Adhesions to Membrane Ruffles.

机构信息

Laboratoire de Biophotonique et Pharmacologie, CNRS, UMR 7213, 74 rte du Rhin, 67401 Illkirch, France.

出版信息

J Oncol. 2010;2010. doi: 10.1155/2010/932803. Epub 2010 Aug 19.

DOI:10.1155/2010/932803
PMID:20847951
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2934852/
Abstract

Cell adhesion and migration are key determinants in tumor metastasis. Adherence of tumor cell to the extracellular matrix is mediated via integrin containing focal adhesions (FAs). Binding of integrins to ECM triggers phosphorylation of two major components of FAs, focal adhesion kinase (FAK) and Src, activating downstream signaling pathway which leads to FA disassembly and cell migration. In this paper, we analyze how phosphorylation of FAK regulates its trafficking at FAs in living human astrocytoma cells. Upon pervanadate-induced FAK phosphorylation, phosphorylated FAK appeared highly expressed at newly formed membrane ruffles. This effect was abolished in presence of the specific Src inhibitor PP2. Our findings demonstrate that upon phosphorylation, FAK delocalizes from FAs to membrane ruffles.

摘要

细胞黏附和迁移是肿瘤转移的关键决定因素。肿瘤细胞与细胞外基质的黏附是通过整合素包含的黏着斑（FA）介导的。整合素与 ECM 的结合触发黏着斑的两个主要成分——黏着斑激酶（FAK）和Src 的磷酸化，激活下游信号通路，导致黏着斑解体和细胞迁移。在本文中，我们分析了 FAK 的磷酸化如何调节其在活的人星形胶质细胞瘤细胞中的 FA 运输。在过钒酸钠诱导的 FAK 磷酸化后，磷酸化的 FAK 高度表达在新形成的膜皱襞中。在存在特异性Src 抑制剂 PP2 的情况下，这种作用被消除。我们的研究结果表明，磷酸化后，FAK 从黏着斑转位到膜皱襞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeae/2934852/43b9af3c28a7/JO2010-932803.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeae/2934852/e02a5097a918/JO2010-932803.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeae/2934852/7dd19fcaf499/JO2010-932803.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeae/2934852/c7b57ceaa5cb/JO2010-932803.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeae/2934852/031101027934/JO2010-932803.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeae/2934852/d94160e315df/JO2010-932803.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeae/2934852/43b9af3c28a7/JO2010-932803.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeae/2934852/e02a5097a918/JO2010-932803.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeae/2934852/7dd19fcaf499/JO2010-932803.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeae/2934852/c7b57ceaa5cb/JO2010-932803.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeae/2934852/031101027934/JO2010-932803.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeae/2934852/d94160e315df/JO2010-932803.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeae/2934852/43b9af3c28a7/JO2010-932803.006.jpg

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A novel small molecule inhibitor of FAK decreases growth of human pancreatic cancer.一种新型的粘着斑激酶小分子抑制剂可降低人胰腺癌的生长。
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Inhibition of focal adhesion kinase as a potential therapeutic strategy for imatinib-resistant gastrointestinal stromal tumor.
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Hepatol Commun. 2019 Dec 20;4(2):268-283. doi: 10.1002/hep4.1452. eCollection 2020 Feb.
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Quercetin Prevents O157:H7 Adhesion to Epithelial Cells via Suppressing Focal Adhesions.槲皮素通过抑制粘着斑来防止O157:H7粘附上皮细胞。
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Orphan G protein-coupled receptor GPRC5A modulates integrin β1-mediated epithelial cell adhesion.孤儿 G 蛋白偶联受体 GPRC5A 调节整合素 β1 介导的上皮细胞黏附。
Cell Adh Migr. 2017 Sep 3;11(5-6):434-446. doi: 10.1080/19336918.2016.1245264. Epub 2017 Feb 6.
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Conformational dynamics of the focal adhesion targeting domain control specific functions of focal adhesion kinase in cells.粘着斑靶向结构域的构象动力学控制着粘着斑激酶在细胞中的特定功能。
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The tumor suppressor gene ARHI (DIRAS3) inhibits ovarian cancer cell migration through multiple mechanisms.抑癌基因 ARHI（DIRAS3）通过多种机制抑制卵巢癌细胞迁移。
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