Role of integrins in cell invasion and migration

Hood, John; Cheresh, David A.

doi:10.1038/nrc727

Cited by 1,578 publications

(1,347 citation statements)

References 115 publications

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“…39 Integrins also play a dominant role in metastasis, a process characterized by altered cancer cell motility and adhesion to surrounding cells and tissues. 40,41 The roles for specific integrins have been described in a number of tumor types, and often multiple integrins are involved within a single tumor type. For example, during attachment to lymph nodes, melanoma cells utilize aVb3-vitronectin binding interactions, whereas breast cancer cells utilize a3b1-fibronectin binding.…”

Section: Discussionmentioning

confidence: 99%

DNAzymes to mouse β1 integrin mRNA in vivo: targeting the tumor vasculature and retarding cancer growth

et al. 2009

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Previously, we designed a DNAzyme (b1DE) targeting the human b1 integrin subunit, which efficiently digested the mRNA of the b1 integrin subunit and downregulated b1 integrin expression in endothelial cells. This DNAzyme blocked the adhesion of endothelial cells and abolished their ability to form microcapillary tubes in Matrigel. In our present study, we demonstrate that b1DE effectively inhibited neovascularization in Matrigel plugs (BALB/c mice, n ¼ 20) and solid human carcinoma tumors developed in nude mice (BALB/cA nude (nu-/-)-B6.Cg-Foxn1 nu ) (n ¼ 30) using prostate carcinoma cells PC-3 (n ¼ 15) and colon adenocarcinoma cells CX1.1 (n ¼ 15). When injected intratumorally, it significantly reduced the tumor size and number of microvessels developed by both CX1.1 and PC-3 cells within the 3 weeks of experiment duration. Thus, DNAzymes targeting b1 integrin genes can inhibit multiple key tumorigenic processes in vitro and in vivo and may serve as useful anti-cancer agents.

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Section: Discussionmentioning

confidence: 99%

DNAzymes to mouse β1 integrin mRNA in vivo: targeting the tumor vasculature and retarding cancer growth

et al. 2009

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“…This is known to occur in other cancers (Taubert et al, 2004) and in many men with malignancy in the prostate and in other genito-urinary cancers (McIntyre et al, 2000;Meye et al, 2002). However, the presence of circulating cells per se does not necessarily lead to metastasis formation (Hood and Cheresh, 2002). The reasons for this are unclear at the present time.…”

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confidence: 82%

Invasive characteristics of human prostatic epithelial cells: understanding the metastatic process

et al. 2005

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Prostate cancer has a predilection to metastasise to the bone marrow stroma (BMS) by an as yet uncharacterised mechanism. We have defined a series of coculture models of invasion, which simulate the blood/BMS boundary and allow the elucidation of the signalling and mechanics of trans-endothelial migration within the complex bone marrow environment. Confocal microscopy shows that prostate epithelial cells bind specifically to bone marrow endothelial-to-endothelial cell junctions and initiate endothelial cell retraction. Trans-endothelial migration proceeds via an epithelial cell pseudopodial process, with complete epithelial migration occurring after 232743 min. Stromal-derived factor-1 (SDF-1)/CXCR4 signalling induced PC-3 to invade across a basement membrane although the level of invasion was 3.5-fold less than invasion towards BMS (P ¼ 0.0007) or bone marrow endothelial cells (P ¼ 0.004). Maximal SDF-1 signalling of invasion was completely inhibited by 10 mM of the SDF-1 inhibitor T140. However, 10 mM T140 only reduced invasion towards BMS and bone marrow endothelial cells by 59% (P ¼ 0.001) and 29% (P ¼ 0.011), respectively. This study highlights the need to examine the potential roles of signalling molecules and/or inhibitors, not just in single-cell models but in coculture models that mimic the complex environment of the bone marrow.

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“…Integrins are the main receptors that mediate cellular interactions with extracellular matrix ligands such as laminins, collagens and fibronectins (Hood and Cheresh, 2002). They are heterodimeric (ab) type I transmembrane receptors, and provide a connection between the matrix and the cytoskeleton.…”

Section: Dependence Receptors: a Short Historymentioning

confidence: 99%

Dependence receptors: a new paradigm in cell signaling and cancer therapy

2010

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Dependence receptors (DRs) now form a family of more than a dozen membrane receptors that are not linked by their structure, but by common functional traits. The most notable is their ability to trigger two opposite signaling pathways: in the presence of ligand, these receptors activate classic signaling pathways implicated in cell survival, migration and differentiation. In the absence of ligand, they do not stay inactive, rather they elicit an apoptotic signal. Thus, cells expressing this kind of receptor are dependent on the presence of ligand in the extracellular environment to survive. This review will recapitulate the increasing data regarding the molecular mechanisms associated with DRs, their potential implication during development, as well as their deregulation during tumorigenesis and, finally, their emergence as new possible therapeutic targets for cancer treatment.

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Role of integrins in cell invasion and migration

Cited by 1,578 publications

References 115 publications

DNAzymes to mouse β1 integrin mRNA in vivo: targeting the tumor vasculature and retarding cancer growth

DNAzymes to mouse β1 integrin mRNA in vivo: targeting the tumor vasculature and retarding cancer growth

Invasive characteristics of human prostatic epithelial cells: understanding the metastatic process

Dependence receptors: a new paradigm in cell signaling and cancer therapy

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