Cell adhesion & migration (Cell Adhes Migrat )

Publisher: Landes Bioscience

Description

In January of 2007 we plan to launch Cell Adhesion & Migration, the first international peer-reviewed journal to focus exclusively on cell-cell and cell-extracellular matrix interactions and their biological consequence on adhesion and migration. Original papers will cover topics important in the field, including assembly of cell adhesion complexes, biological functions and molecular interactions of ECM molecules, cytoskeleton plasticity and related signalling cascades, cell fusion, immune synapse formation or axon growth and guidance both in physiological condition such as organogenesis and development (special attention will be paid to papers related to stem cells migration or cell intercalation) or pathological conditions such as cancer cell migration or degenerative diseases.

Impact factor 3.40

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    Impact factor
  • 5-year impact
    2.30
  • Cited half-life
    3.00
  • Immediacy index
    0.54
  • Eigenfactor
    0.01
  • Article influence
    0.89
  • Website
    Cell Adhesion & Migration website
  • Other titles
    Cell adhesion & migration
  • ISSN
    1933-6926
  • OCLC
    71757501
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Landes Bioscience

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors final version only
    • On Institutional Repositories
    • Must link to publisher version
    • Published source must be acknowledged
    • Landes Bioscience will deposit in PubMed Central or Europe PMC within 6-12 months of publication, depending on funding agency policy
    • Embargoes on funding agency requirements, can be removed by payment of Open Access fee
    • Publisher's version/PDF cannot be used
  • Classification
    ​ blue

Publications in this journal

  • Bao-Zhang Guan, Rui-Ling Yan, Jian-Wei Huang, Fo-Lan Li, Ying-Xue Zhong, Yu Chen, Fan-Na Liu, Bo Hu, Si-Bo Huang, Liang-Hong Yin
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    ABSTRACT: ABSTRACT Renal cell carcinoma (RCC) is the third most frequent malignancy within urological oncology. However, the mechanisms responsible for RCC metastasis are still needed further illustration. Our present study revealed that a seven-transmembrane receptor G-protein coupled estrogen receptor (GPER) was highly detected in various RCC cell lines such as ACHN, OS-RC-2 and SW839. The activation of GPER by its specific agonist G-1 significantly promoted the in vitro migration and invasion of ACHN and OS-RC-2 cells. G-1 also up regulated the expression of matrix metalloproteinase-2 (MMP-2) and MMP-9. The inhibitor of MMP-9 (Cat-444278), but not MMP-2 (Sc-204092), abolished G-1 induced cell migration, which suggested that MMP-9 is the key molecule mediating G-1 induced RCC progression. Further, G-1 treatment resulted in phosphorylation of AKT and ERK in RCC cells. PI3K/AKT inhibitor (LY294002), while not ERK inhibitor (PD98059), significantly abolished G-1 induced up regulation of MMP-9 in both AHCN and OS-RC-2 cells. Generally, our data revealed that activation of GPER by its specific agonist G-1 promoted the metastasis of RCC cells through PI3K/AKT/MMP-9 signals, which might be a promising new target for drug discovery of RCC patients.
    Cell adhesion & migration 01/2015;
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    ABSTRACT: Abstract Despite an increasing knowledge about the causes of cancer, this disease is difficult to cure and still causes far too high a death rate. Based on advances in our understanding of disease pathogenesis, novel treatment concepts, including targeting the tumor microenvironment, have been developed and are being combined with established treatment regimens such as surgical removal and radiotherapy. Yet it is obvious that we need additional strategies to prevent tumor relapse and metastasis. Given its exceptional high expression in most cancers with low abundance in normal tissues, tenascin-C appears an ideal candidate for tumor treatment. Here, we will summarize the current applications of targeting tenascin-C as a treatment for different tumors, and highlight the potential of this therapeutic approach.
    Cell adhesion & migration 01/2015;
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    ABSTRACT: Abstract Fetal variants of tenascin-C are not expressed in healthy adult myocardium. But, there is a relevant re-occurrence during pathologic cardiac tissue and vascular remodelling. Thus, these molecules, in particular B and C domain containing tenascin-C, might qualify as promising novel biomarkers for diagnosis and prognosis estimation. Since a stable extracellular deposition of fetal tenascin-C variants is present in diseased cardiac tissue, the molecules are excellent target structures for antibody-based delivery of diagnostic (e.g., radionuclides) or therapeutic (bioactive payloads) agents directly to the site of disease. Against the background that fetal tenascin-C variants are functionally involved in cardiovascular tissue remodelling, therapeutic functional blocking strategies could be experimentally tested in the future.
    Cell adhesion & migration 01/2015;
  • Chiara Catania, Michela Maur, Rossana Berardi, Andrea Rocca, Anna Maria Di Giacomo, Gianluca Spitaleri, Cristina Masini, Chiara Pierantoni, Reinerio González-Iglesias, Giulia Zigon, Annaelisa Tasciotti, Leonardo Giovannoni, Valeria Lovato, Giuliano Elia, Hans D Menssen, Dario Neri, Stefano Cascinu, Pier Franco Conte, Filippo de Braud
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    ABSTRACT: A phase Ib/II trial was performed to evaluate safety, tolerability, recommended dose (RD) and efficacy of F16-IL2, a recombinant antibody-cytokine fusion protein, in combination with doxorubicin in patients with solid tumours (phase Ib) and metastatic breast cancer (phase II). Six patient cohorts with progressive solid tumours (n = 19) received escalating doses of F16-IL2 [5-25 Million International Units (MIU) of IL2 equivalent dose] in combination with escalating doses of doxorubicin (0-25mg/m(2)) on day 1, 8 and 15 every 4 weeks. Subsequently, patients with metastatic breast cancer (n = 10) received the drug combination at the RD. Clinical data and laboratory findings were analysed for safety, tolerability, and activity. F16-IL2 could be administered up to 25 MIU, in combination with the RD of doxorubicin (25mg/m(2)). No human anti-fusion protein antibodies (HAFA) response was detected. Pharmacokinetics of F16-IL2 was dose-dependent over the tested range, with half-lives of ca. 13 and ca. 8 hours for cohorts dosed at lower and higher levels, respectively. Toxicities were controllable and reversible, with no combination treatment-related death. After 8 weeks, 57% and 67% disease control rates were observed for Phase I and II, respectively (decreasing to 43% and 33% after 12 weeks), considering 14 and 9 patients evaluable for efficacy. One patient experienced a long lasting partial response (45 weeks), still on-going at exit of study. F16-IL2 can be safely and repeatedly administered at the RD of 25 Mio I.U. in combination with 25mg/m(2) doxorubicin; its safety and activity are currently being investigated in combination with other chemotherapeutics, in order to establish optimal therapy settings.
    Cell adhesion & migration 01/2015;
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    ABSTRACT: Previous studies from our lab have shown that both boric (BA) and phenylboronic- acid (PBA) inhibit the migration of prostate cancer cell lines, as well as non-tumorigenic prostate cells. Our results indicate that PBA is more potent than BA in targeting metastatic and proliferative properties of cancer cells. Here we focus on the impact of BA and PBA on Rho family of GTP-binding proteins and their downstream targets. Treatment with 1mM PBA and BA decreases activities of RhoA, Rac1, and Cdc42 in DU-145 metastatic prostate cancer cells, but not in normal RWPE-1 prostate cells. Furthermore, ROCKII activity and phosphorylation of myosin light chain kinase decrease as a result of either PBA or BA treatment in DU-145 cells, suggesting these compounds target actomyosin-based contractility.
    Cell adhesion & migration 10/2014; 5(5):382-6.
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    ABSTRACT: Most cells in the body secrete, or are in intimate contact with extracellular matrix (ECM), which provides structure to tissues and regulates various cellular phenotypes. Cells are well known to respond to biochemical signals from the ECM, but recent evidence has highlighted the mechanical properties of the matrix, including matrix elasticity and nanotopography, as fundamental instructive cues regulating signal transduction pathways and gene transcription. Recent observations also highlight the importance of matrix nanotopography as a regulator of cellular functions, but lack of facile experimental platforms has resulted in a continued negligence of this important microenvironmental cue in tissue culture experimentation. In this review, we present our opinion on the importance of nanotopography as a biological cue, contexts in which it plays a primary role influencing cell behavior, and detail advanced techniques to incorporate nanotopography into the design of experiments, or in cell culture environments. In addition, we highlight signal transduction pathways that are involved in conveying the extracellular matrix nanotopography information within the cells to influence cell behavior.
    Cell adhesion & migration 07/2014; 8(4).
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    ABSTRACT: Fibrillin-1 is a microfibrillar extracellular matrix protein that was described to be a ligand for α8 integrin. α8 integrin is a matrix receptor specifically expressed in mesangial and smooth muscle cells of the kidney. In previous studies we detected glomerular expression of fibrillin-1. Moreover, fibrillin-1 promoted adhesion, migration, and proliferation of mesangial cells. We hypothesized that fibrillin-1 and α8 integrin might interact in the glomerulus, and thus, regulate mesangial cell properties. Our studies showed that fibrillin-1 and α8 integrin colocalize in the glomerular mesangium. Induction of experimental glomerulonephritis led to an increase of both fibrillin-1 and α8 integrin expression. In vitro studies revealed that mesangial cells deficient for α8 integrin adhere weaker to fibrillin-1 and migrate more easily on fibrillin-1 than wild-type mesangial cells. Baseline proliferation on fibrillin-1 is higher in α8 integrin-deficient mesangial cells, but the induction of proliferation is not different in α8 integrin-deficient and wild-type mesangial cells. We conclude that fibrillin-1 and α8 integrin interact, and thus, regulate mesangial cell adhesion and migration. The concomitant induction of both fibrillin-1 and α8 integrin in a self-limited model of glomerular injury point to a protective role of the interaction of fibrillin-1 with α8 integrin in the glomerulus resulting in reduced damage of the glomerular tuft as a consequence of firm adhesion of mesangial cells.
    Cell adhesion & migration 05/2014; 8(4).
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    ABSTRACT: Systems biology has recently achieved significant success in the understanding of complex interconnected phenomena such as cell polarity and migration. In this context, the definition of systems biology has come to encompass the integration of quantitative measurements with sophisticated modeling approaches. This article will review recent progress in live cell imaging technologies that have expanded the possibilities of quantitative in vivo measurements, particularly in regards to molecule counting and quantitative measurements of protein concentration and dynamics. These methods have gained and continue to gain popularity with the biological community. In general, we will discuss three broad categories: protein interactions, protein quantitation, and protein dynamics.
    Cell adhesion & migration 05/2014; 8(4):1-10.
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    ABSTRACT: The vasculature delivers vital support for all other tissues by supplying oxygen and nutrients for growth and by transporting the immune cells that protect and cure them. Therefore, the microvasculature developed a special barrier that is permissive for gasses like oxygen and carbon dioxide, while fluids are kept inside and pathogens are kept out. While maintaining this tight barrier, the vascular wall also allows immune cells to exit at sites of inflammation or damage, a process that is called transmigration. The endothelial cell layer that forms the inner lining of the vasculature is crucial for the vascular barrier function as well as the regulation of transmigration. Therefore, adhesions between vascular endothelial cells are both tight and dynamic and the mechanisms by which they are established, and the mechanisms by which they are controlled have been extensively studied over the past decades. Because of our fundamental strive to understand biology, but also because defects in vascular barrier control cause a variety of clinical problems and treatment strategies may evolve from our detailed understanding of its mechanisms. This special focus issue features a collection of articles that review key components of the development and control of the endothelial cell-cell junction that is central to endothelial barrier function.
    Cell adhesion & migration 05/2014; 8(2).
  • Cell adhesion & migration 04/2014; 8(3).
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    ABSTRACT: Basement membranes are thin sheets of self-assembled extracellular matrices that are essential for embryonic development and for the homeostasis of adult tissues. They play a role in structuring, protecting, polarizing, and compartmentalizing cells, as well as in supplying them with growth factors. All basement membranes are built from laminin and collagen IV networks stabilized by nidogen/perlecan bridges. The precise composition of basement membranes, however, varies between different tissues. Even though basement membranes represent physical barriers that delimit different tissues, they are breached in many physiological or pathological processes, including development, the immune response, and tumor invasion. Here, we provide a brief overview of the molecular composition of basement membranes and the process of their assembly. We will then illustrate the heterogeneity of basement membranes using two examples, the epithelial basement membrane in the gut and the vascular basement membrane. Finally, we examine the different strategies cells use to breach the basement membrane.
    Cell adhesion & migration 04/2014; 8(3).
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    ABSTRACT: Invadosomes have two main functions represented by their actin-rich and adhesive components and their polarized secretory pathways controlling the delivery of metalloproteases necessary to degrade extracellular matrix (ECM). Invadosomes include invadopodia and podosomes, which have subtle differences in molecular composition, dynamics, and structure. These differences could reflect different stages of invadosome maturation. This review will outline current knowledge on the coupling between the acto-adhesive machinery and the ECM degradation activity in invadosome diversity. Multiple works support that these two functions are not automatically linked but seem to be finely regulated to allow different functions of invadosomes. We will explore the paradigmatic aspect of invadosomes, which are able to interact with ECM to degrade it so as to better control their own dynamics. Understanding the fine-tuning between these two functions could serve to understand the link between the different types of invadosomes from invadopodia to podosomes.
    Cell adhesion & migration 04/2014; 8(3).
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    ABSTRACT: Cell migration is a highly regulated multistep process that requires the coordinated regulation of cell adhesion, protrusion, and contraction. These processes require numerous protein-protein interactions and the activation of specific signaling pathways. The Rho family of GTPases plays a key role in virtually every aspect of the cell migration cycle. The activation of Rho GTPases is mediated by a large and diverse family of proteins; the guanine nucleotide exchange factors (RhoGEFs). GEFs work immediately upstream of Rho proteins to provide a direct link between Rho activation and cell-surface receptors for various cytokines, growth factors, adhesion molecules, and G protein-coupled receptors. The regulated targeting and activation of RhoGEFs is essential to coordinate the migratory process. In this review, we summarize the recent advances in our understanding of the role of RhoGEFs in the regulation of cell migration.
    Cell adhesion & migration 04/2014; 8(4).
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    ABSTRACT: The small GTPase Rab5 has been extensively studied in the context of endocytic trafficking because it is critical in the regulation of early endosome dynamics. In addition to this canonical role, evidence obtained in recent years implicates Rab5 in the regulation of cell migration. This novel role of Rab5 is based not only on an indirect relationship between cell migration and endosomal trafficking as separate processes, but also on the direct regulation of signaling proteins implicated in cell migration. However, the precise mechanisms underlying this connection have remained elusive. Recent studies have shown that the activation of Rab5 is a critical event for maintaining the dynamics of focal adhesions, which is fundamental in regulating not only cell migration but also tumor cell invasion.
    Cell adhesion & migration 04/2014; 8(2).
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    ABSTRACT: The homeostatic function of endothelial cells (EC) is critical for a number of physiological processes including vascular integrity, immunity, and wound healing. Indeed, vascular abnormalities resulting from EC dysfunction contribute to the development and spread of malignancies. The alternative SDF-1/CXCL12 receptor CXCR7 is frequently and specifically highly expressed in tumor-associated vessels. In this study, we investigate whether CXCR7 contributes to vascular dysfunction by specifically examining the effect of CXCR7 expression on EC barrier function and motility. We demonstrate that CXCR7 expression in EC results in redistribution of CD31/PECAM-1 and loss of contact inhibition. Moreover, CXCR7+ EC are deficient in barrier formation. We show that CXCR7-mediated motility has no influence on angiogenesis but contributes to another motile process, the invasion of CXCR7+ EC into ligand-rich niches. These results identify CXCR7 as a novel manipulator of EC barrier function via alteration of PECAM-1 homophilic junctions. As such, aberrant expression of CXCR7 in the vasculature has the potential to disrupt vascular homeostasis and could contribute to vascular dysfunction in cancer systems.
    Cell adhesion & migration 03/2014; 8(2).
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    ABSTRACT: Over 20 years ago, protrusive, F-actin-based membrane structures, termed invadopodia, were identified in highly metastatic cancer cell lines. Invadopodia penetrate artificial or explanted extracellular matrices in 2D culture conditions and have been hypothesized to facilitate the migration of cancer cells through basement membrane, a thin, dense, barrier-like matrix surrounding most tissues. Despite intensive study, the identification of invadopodia in vivo has remained elusive and until now their possible roles during invasion or even existence have remained unclear. Studies in remarkably different cellular contexts-mouse tumor models, zebrafish intestinal epithelia, and C. elegans organogenesis-have recently identified invadopodia structures associated with basement membrane invasion. These studies are providing the first in vivo insight into the regulation, function, and role of these fascinating subcellular devices with critical importance to both development and human disease.
    Cell adhesion & migration 03/2014; 8(3).