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本文引用的文献

1
Palladin promotes invasion of pancreatic cancer cells by enhancing invadopodia formation in cancer-associated fibroblasts.Palladin 通过增强癌相关成纤维细胞中的侵袭伪足形成促进胰腺癌的侵袭。
Oncogene. 2014 Mar 6;33(10):1265-73. doi: 10.1038/onc.2013.68. Epub 2013 Mar 25.
2
WIP: WASP-interacting proteins at invadopodia and podosomes.正在进行的工作:参与侵袭伪足和足突的 WASP 相互作用蛋白。
Eur J Cell Biol. 2012 Nov-Dec;91(11-12):869-77. doi: 10.1016/j.ejcb.2012.06.002. Epub 2012 Jul 21.
3
Pathological roles of invadopodia in cancer invasion and metastasis.侵袭伪足在癌症侵袭和转移中的病理作用。
Eur J Cell Biol. 2012 Nov-Dec;91(11-12):902-7. doi: 10.1016/j.ejcb.2012.04.005. Epub 2012 Jun 2.
4
Met receptor tyrosine kinase signals through a cortactin-Gab1 scaffold complex, to mediate invadopodia.表皮生长因子受体酪氨酸激酶通过衔接蛋白 Gab1 与细胞骨架蛋白 cortactin 形成复合物,进而调节侵袭伪足的形成。
J Cell Sci. 2012 Jun 15;125(Pt 12):2940-53. doi: 10.1242/jcs.100834. Epub 2012 Feb 24.
5
Arousal of cancer-associated stroma: overexpression of palladin activates fibroblasts to promote tumor invasion.激活肿瘤相关基质:palladin 的过表达激活成纤维细胞促进肿瘤侵袭。
PLoS One. 2012;7(1):e30219. doi: 10.1371/journal.pone.0030219. Epub 2012 Jan 23.
6
Elevated expression of stromal palladin predicts poor clinical outcome in renal cell carcinoma.间质层联蛋白表达升高预示肾细胞癌患者临床预后不良。
PLoS One. 2011;6(6):e21494. doi: 10.1371/journal.pone.0021494. Epub 2011 Jun 28.
7
Phosphoinositide 3-kinase signaling pathway mediated by p110α regulates invadopodia formation.磷酸肌醇 3-激酶信号通路通过 p110α 调节侵袭伪足的形成。
J Cell Biol. 2011 Jun 27;193(7):1275-88. doi: 10.1083/jcb.201009126.
8
The 'ins' and 'outs' of podosomes and invadopodia: characteristics, formation and function.足突和侵袭伪足的“内部”和“外部”:特征、形成和功能。
Nat Rev Mol Cell Biol. 2011 Jun 23;12(7):413-26. doi: 10.1038/nrm3141.
9
Invadosome regulation by adhesion signaling.侵袭伪足形成的黏附信号调控。
Curr Opin Cell Biol. 2011 Oct;23(5):597-606. doi: 10.1016/j.ceb.2011.04.002. Epub 2011 May 6.
10
Twist1-induced invadopodia formation promotes tumor metastasis.Twist1 诱导的侵袭伪足形成促进肿瘤转移。
Cancer Cell. 2011 Mar 8;19(3):372-86. doi: 10.1016/j.ccr.2011.01.036.

帕拉丁调节癌症侵袭所需的肌动蛋白结构。

Palladin regulation of the actin structures needed for cancer invasion.

机构信息

Department of Natural Sciences; Lebanese American University; Beirut, Lebanon.

出版信息

Cell Adh Migr. 2014;8(1):29-35. doi: 10.4161/cam.28024. Epub 2013 Jan 1.

DOI:10.4161/cam.28024
PMID:24525547
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3974790/
Abstract

Cell migration and invasion involve the formation of cell adhesion structures as well as the dynamic and spatial regulation of the cytoskeleton. The adhesive structures known as podosomes and invadopodia share a common role in cell motility, adhesion, and invasion, and form when the plasma membrane of motile cells undergoes highly regulated protrusions. Palladin, a molecular scaffold, co-localizes with actin-rich structures where it plays a role in their assembly and maintenance in a wide variety of cell lines. Palladin regulates actin cytoskeleton organization as well as cell adhesion formation. Moreover, palladin contributes to the invasive nature of cancer metastatic cells by regulating invadopodia formation. Palladin seems to regulate podosome and invodopodia formation through Rho GTPases, which are known as key players in coordinating the cellular responses required for cell migration and metastasis.

摘要

细胞迁移和入侵涉及细胞黏附结构的形成,以及细胞骨架的动态和空间调节。被称为 podosomes 和 invadopodia 的黏附结构在细胞运动、黏附和入侵中发挥共同作用,并且在运动细胞的质膜发生高度调节的突起时形成。palladin 是一种分子支架,与富含肌动蛋白的结构共定位,在多种细胞系中发挥作用,调节它们的组装和维持。palladin 调节肌动蛋白细胞骨架组织以及细胞黏附的形成。此外,palladin 通过调节侵袭小体的形成,促进癌症转移细胞的侵袭特性。palladin 似乎通过 Rho GTPases 调节 podosome 和 invodopodia 的形成,Rho GTPases 是协调细胞迁移和转移所需的细胞反应的关键参与者。