Signaling pathways and cell mechanics involved in wound closure by epithelial cell sheets

Fenteany, Gabriel; Janmey, Paul A.; Stossel, Thomas P.

doi:10.1016/s0960-9822(00)00579-0

Cited by 282 publications

(292 citation statements)

References 30 publications

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“…Namely, Taniuchi et al (2005) showed that a pancreatic cancer cell line, transfected with wild-type P-cadherin, migrated faster than the cells without this molecule. Epithelial cell migration requires the coordination of three basic cellular processes: actin cytoskeleton reorganization, matrix adhesion and matrix re-modelling (Lauffenburger and Horwitz, 1996;Fenteany et al, 2000). In this present study, we also show, by time-lapse microscopy and actin phalloidin staining, that P-cadherin is able to induce phenotypic changes involving alterations in cell polarity and leading edge morphology, formation of membrane protrusions, as well as, increase of their cytoplasmic area, which usually is characteristic from cells with a motile behaviour.…”

Section: Discussionmentioning

confidence: 99%

Extracellular cleavage and shedding of P-cadherin: a mechanism underlying the invasive behaviour of breast cancer cells

et al. 2009

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Cell-cell adhesion is an elementary process in normal epithelial cellular architecture. Several studies have shown the role mediated by cadherins in this process, besides their role in the maintenance of cell polarity, differentiation and cell growth. However, during tumour progression, these molecules are frequently altered. In breast cancer, tumours that overexpress P-cadherin usually present a high histological grade, show decreased cell polarity and are associated with worse patient survival. However, little is known about how this protein dictates the very aggressive behaviour of these tumours. To achieve this goal, we set up two breast cancer cell models, where P-cadherin expression was differently modulated and analysed in terms of cell invasion, motility and migration. We show that P-cadherin overexpression, in breast cancer cells with wild-type E-cadherin, promotes cell invasion, motility and migration. Moreover, we found that the overexpression of P-cadherin induces the secretion of matrix metalloproteases, specifically MMP-1 and MMP-2, which then lead to P-cadherin ectodomain cleavage. Further, we showed that soluble P-cadherin fragment is able to induce in vitro invasion of breast cancer cells. Overall, our results contribute to elucidate the mechanism underlying the invasive behaviour of P-cadherin expressing breast tumours.

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Section: Discussionmentioning

confidence: 99%

Extracellular cleavage and shedding of P-cadherin: a mechanism underlying the invasive behaviour of breast cancer cells

et al. 2009

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“…There are some significant distinctions of size, speed, and degree of cellularization that make closure of the Xenopus cleavage furrow an interesting process to investigate. For example, compared with in vivo wound closure models such as corneal epithelium (Matsuda et al, 1985) or Xenopus tadpole tail (Radice, 1980), in which free margins typically advance in the range of 2-10 m/min, respectively, or in vitro models such as monolayered MDCK cells, which may be 10 -100ϫ slower yet (Fenteany et al, 2000), closure of the Xenopus embryo cleavage furrow proceeds with extreme rapidity. Zippering by the first cleavage furrow closes a 1-mm opening in approximately 15 min.…”

Section: Discussionmentioning

confidence: 99%

Membrane dynamics of cleavage furrow closure in Xenopus laevis

Danilchik

Brown

2008

Developmental Dynamics

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“…Differences among cell types, coupled with the participation of Cdc42 in cell-cell adhesion [38], further complicate the issue. For example, Cdc42 is not required for wound closure by Madin-Darby canine kidney (MDCK) cells [39]. In addition to inducing the formation of filopodia, Cdc42 regulates cell polarity during movement [40].…”

Section: Discussionmentioning

confidence: 99%

Multiple proteins mediate IQGAP1-stimulated cell migration

Mataraza

Jeong

et al. 2007

Cellular Signalling

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Cell migration, a highly complex physiological phenomenon that requires the co-ordinated and tightly regulated function of several proteins, is mediated by a number of signalling pathways. Elucidation of the molecular mechanisms of cell migration impacts our comprehension of numerous cell functions, ranging from development and immune surveillance to angiogenesis and metastasis. The scaffold protein IQGAP1, which binds multiple proteins and regulates their functions, promotes cell motility. Many of the IQGAP1 binding proteins have been implicated in cell migration. In this study, we employed a multifaceted strategy to identify proteins that contribute to IQGAP1-stimulated cell migration. Using specific IQGAP1 point mutant constructs, an interaction with actin was shown to be essential for IQGAP1 to increase cell migration. In contrast, eliminating the binding of Ca 2+ / calmodulin, but not Ca 2+ -free calmodulin, augmented the ability of IQGAP1 to stimulate cell migration. Consistent with these findings, selective inhibition of calmodulin function at the plasma membrane with a specific peptide inhibitor enhanced cell migration mediated by IQGAP1. Interestingly, immunofluorescence staining and confocal microscopy suggest that localization of Cdc42 at the leading edge is not necessary for maximal migration of epithelial cells. Coupled with the observations that Cdc42 and Rac1 contribute to IQGAP1-stimulated cell migration, these data suggest that IQGAP1 serves as a junction to integrate multiple signalling molecules to facilitate cell migration.

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Signaling pathways and cell mechanics involved in wound closure by epithelial cell sheets

Cited by 282 publications

References 30 publications

Extracellular cleavage and shedding of P-cadherin: a mechanism underlying the invasive behaviour of breast cancer cells

Extracellular cleavage and shedding of P-cadherin: a mechanism underlying the invasive behaviour of breast cancer cells

Membrane dynamics of cleavage furrow closure in Xenopus laevis

Multiple proteins mediate IQGAP1-stimulated cell migration

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