Yamaguchi Hideki, Pixley Fiona, Condeelis John
Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY10461, USA.
Eur J Cell Biol. 2006 Apr;85(3-4):213-8. doi: 10.1016/j.ejcb.2005.10.004. Epub 2005 Nov 8.
Cell migration through the extracellular matrix (ECM) is necessary for cancer cells to invade adjacent tissues and metastasize to an organ distant from primary tumors. Highly invasive carcinoma cells form ECM-degrading membrane protrusions called invadopodia. Tumor-associated macrophages have been shown to promote the migratory phenotypes of carcinoma cells, and macrophages are known to form podosomes, similar structures to invadopodia. However, the role of invadopodia and podosomes in vivo remains to be determined. In this paper, we propose a model for possible functions and interactions of invadopodia and podosomes in tumor invasion, based on observations that macrophage podosomes degrade ECM and that podosome formation is regulated by colony-stimulating factor-1 signaling.
癌细胞通过细胞外基质(ECM)迁移对于其侵袭邻近组织并转移至远离原发肿瘤的器官是必要的。高侵袭性癌细胞会形成被称为侵袭伪足的降解ECM的膜状突起。肿瘤相关巨噬细胞已被证明可促进癌细胞的迁移表型,并且已知巨噬细胞会形成与侵袭伪足类似结构的足体。然而,侵袭伪足和足体在体内的作用仍有待确定。在本文中,基于巨噬细胞足体可降解ECM以及足体形成受集落刺激因子-1信号调控的观察结果,我们提出了一个关于侵袭伪足和足体在肿瘤侵袭中可能的功能及相互作用的模型。