Improving Fluorescence-Based Assays for the In Vitro Analysis of Cell Adhesion and Migration

2002 ◽  
Vol 20 (3) ◽  
pp. 285-304 ◽  
Author(s):  
Paola Spessotto ◽  
Emiliana Giacomello ◽  
Roberto Perris
Keyword(s):  
Cell Adhesion ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Vitro Analysis ◽  
In Vitro Analysis

Fluorescence-Based Assays for In Vitro Analysis of Cell Adhesion and Migration

2009 ◽  
pp. 221-250 ◽  
Author(s):  
Paola Spessotto ◽  
Katia Lacrima ◽  
Pier Andrea Nicolosi ◽  
Eliana Pivetta ◽  
Martina Scapolan ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Vitro Analysis ◽  
In Vitro Analysis

Amygdalin Modulates Prostate Cancer Cell Adhesion and Migration In Vitro

2019 ◽  
Vol 72 (3) ◽  
pp. 528-537 ◽  
Author(s):  
Jens Mani ◽  
Jens Neuschäfer ◽  
Christian Resch ◽  
Jochen Rutz ◽  
Sebastian Maxeiner ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Adhesion ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Adhesion ◽  
Cell Adhesion And Migration ◽  
And Migration

scholarly journals Neural crest cell migration: requirements for exogenous fibronectin and high cell density.

1983 ◽  
Vol 96 (2) ◽  
pp. 462-473 ◽  
Author(s):  
R A Rovasio ◽  
A Delouvee ◽  
K M Yamada ◽  
R Timpl ◽  
J P Thiery
Keyword(s):  
Cell Adhesion ◽  
Neural Crest ◽  
Type I Collagen ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Type I ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Crest Cell

Cells of the neural crest participate in a major class of cell migratory events during embryonic development. From indirect evidence, it has been suggested that fibronectin (FN) might be involved in these events. We have directly tested the role of FN in neural crest cell adhesion and migration using several in vitro model systems. Avian trunk neural crest cells adhered readily to purified plasma FN substrates and to extracellular matrices containing cellular FN. Their adhesion was inhibited by antibodies to a cell-binding fragment of FN. In contrast, these cells did not adhere to glass, type I collagen, or to bovine serum albumin in the absence of FN. Neural crest cell adhesion to laminin (LN) was significantly less than to FN; however, culturing of crest cells under conditions producing an epithelioid phenotype resulted in cells that could bind equally as well to LN as to FN. The migration of neural crest cells appeared to depend on both the substrate and the extent of cell interactions. Cells migrated substantially more rapidly on FN than on LN or type I collagen substrates; if provided a choice between stripes of FN and glass or LN, cells migrated preferentially on the FN. Migration was inhibited by antibodies against the cell-binding region of FN, and the inhibition could be reversed by a subsequent addition of exogenous FN. However, the migration on FN was random and displayed little persistence of direction unless cells were at high densities that permitted frequent contacts. The in vitro rate of migration of cells on FN-containing matrices was 50 microns/h, similar to their migration rates along the narrow regions of FN-containing extracellular matrix in migratory pathways in vivo. These results indicate that FN is important for neural crest cell adhesion and migration and that the high cell densities of neural crest cells in the transient, narrow migratory pathways found in the embryo are necessary for effective directional migration.

scholarly journals Abi1 gene silencing by short hairpin RNA impairs Bcr-Abl-induced cell adhesion and migration in vitro and leukemogenesis in vivo

2008 ◽  
Vol 29 (9) ◽  
pp. 1717-1724 ◽  
Author(s):  
W. Yu ◽  
X. Sun ◽  
N. Clough ◽  
E. Cobos ◽  
Y. Tao ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Gene Silencing ◽  
Short Hairpin Rna ◽  
Hairpin Rna ◽  
Cell Adhesion And Migration ◽  
Short Hairpin ◽  
And Migration

scholarly journals Recreation of the terminal events in physiological integrin activation

2010 ◽  
Vol 188 (1) ◽  
pp. 157-173 ◽  
Author(s):  
Feng Ye ◽  
Guiqing Hu ◽  
Dianne Taylor ◽  
Boris Ratnikov ◽  
Andrey A. Bobkov ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Adhesion ◽  
Integrin Signaling ◽  
Integrin Activation ◽  
Matrix Assembly ◽  
Integrin Αiibβ3 ◽  
Terminal Events ◽  
Cell Adhesion And Migration ◽  
And Migration

Increased affinity of integrins for the extracellular matrix (activation) regulates cell adhesion and migration, extracellular matrix assembly, and mechanotransduction. Major uncertainties concern the sufficiency of talin for activation, whether conformational change without clustering leads to activation, and whether mechanical force is required for molecular extension. Here, we reconstructed physiological integrin activation in vitro and used cellular, biochemical, biophysical, and ultrastructural analyses to show that talin binding is sufficient to activate integrin αIIbβ3. Furthermore, we synthesized nanodiscs, each bearing a single lipid-embedded integrin, and used them to show that talin activates unclustered integrins leading to molecular extension in the absence of force or other membrane proteins. Thus, we provide the first proof that talin binding is sufficient to activate and extend membrane-embedded integrin αIIbβ3, thereby resolving numerous controversies and enabling molecular analysis of reconstructed integrin signaling.

scholarly journals ANGPTL4 overexpression inhibits tumor cell adhesion and migration and predicts favorable prognosis of triple-negative breast cancer

2020 ◽  
Author(s):  
Yu-Chen Cai ◽  
Hang Yang ◽  
Ke-Feng Wang ◽  
Tan-Huan Chen ◽  
Wen-Qi Jiang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Migration And Invasion ◽  
Tumor Cell Adhesion ◽  
Tumor Tissues ◽  
Cell Adhesion And Migration ◽  
And Migration

Abstract Background: Triple-negative breast cancer (TNBC) patients have relatively poor clinical outcomes. A marker predicting the prognosis of patients with TNBC could help guide treatment. Extensive evidence demonstrates that angiopoietin-like 4 (ANGPTL4) is involved in the regulation of cancer growth, metastasis and angiogenesis. Therefore, its role in TNBC is of interest.Methods: We tested the ANGPTL4 expression level in tumor tissues by immunohistochemistry (IHC) and detected its association with the clinical features of TNBC patients. Next, the effects and mechanisms of ANGPTL4 on TNBC cell migration and adhesion were investigated.Results: We found that ANGPTL4 overexpression was associated with favorable outcomes in TNBC patients. ANGPTL4 upregulation inhibited cell adhesion, migration and invasion in vitro. Further analyses demonstrated that the possible mechanism might involve suppression of TNBC progression by interacting with extracellular matrix-related genes.Conclusions: The present findings demonstrated that enhancement of ANGPTL4 expression might inversely correlate with TNBC progression. ANGPTL4 is a promising marker of TNBC and should be evaluated in further studies. Trial registration: Retrospectively registered.

scholarly journals ANGPTL4 overexpression inhibits tumor cell adhesion and migration and predicts favorable prognosis of triple-negative breast cancer

2020 ◽  
Author(s):  
Yu-Chen Cai ◽  
Hang Yang ◽  
Ke-Feng Wang ◽  
Tan-Huan Chen ◽  
Wen-Qi Jiang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Migration And Invasion ◽  
Tumor Cell Adhesion ◽  
Tumor Tissues ◽  
Cell Adhesion And Migration ◽  
And Migration

Abstract Background: Triple-negative breast cancer (TNBC) patients have relatively poor clinical outcomes. A marker predicting the prognosis of patients with TNBC could help guide treatment. Extensive evidence demonstrates that angiopoietin-like 4 (ANGPTL4) is involved in the regulation of cancer growth, metastasis and angiogenesis. Therefore, its role in TNBC is of interest.Methods: We tested the ANGPTL4 expression level in tumor tissues by immunohistochemistry (IHC) and detected its association with the clinical features of TNBC patients. Next, the effects and mechanisms of ANGPTL4 on TNBC cell migration and adhesion were investigated.Results: We found that ANGPTL4 overexpression was associated with favorable outcomes in TNBC patients. ANGPTL4 upregulation inhibited cell adhesion, migration and invasion in vitro. Further analyses demonstrated that the possible mechanism might involve suppression of TNBC progression by interacting with extracellular matrix-related genes.Conclusions: The present findings demonstrated that enhancement of ANGPTL4 expression might inversely correlate with TNBC progression. ANGPTL4 is a promising marker of TNBC and should be evaluated in further studies. Trial registration: Retrospectively registered.

Proteolysis, Cell Adhesion, Chemotaxis, and Invasiveness Are Regulated by the u-PA-u-PAR-PAI-1 System

1999 ◽  
Vol 82 (08) ◽  
pp. 298-304 ◽  
Author(s):  
Francesco Blasi
Keyword(s):  
Cell Adhesion ◽  
Plasminogen Activator ◽  
Tyrosine Kinases ◽  
Plasminogen Activator Inhibitor ◽  
Prognostic Indicators ◽  
Type Plasminogen Activator ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Pai 1

IntroductionHigh levels of urokinase-type plasminogen activator (u-PA), of its inhibitor (plasminogen activator inhibitor (PAI)-1), or of its receptor (u-PAR, CD87) are strong prognostic indicators of relapse in human cancers. In addition, many in vitro data show that u-PA, PAI-1, and u-PAR have a profound influence on cell migration. This set of molecules regulates surface proteolysis, cell adhesion, and chemotaxis through different mechanisms. Binding to u-PAR strongly stimulates the activation of pro-u-PA and, hence, of plasminogen, resulting in localized production of the broad-spectrum serine protease, plasmin, which can digest extracellular matrix proteins or activate latent motogenic factors. Chemotaxis is induced through an u-PA-dependent conformational change in u-PAR, which uncovers a very potent chemotactic epitope(s) that acts through a pertussis toxin-sensitive step and activates intracellular tyrosine kinases. In addition, cell adhesion is affected by an u-PA-dependent exposure of u-PAR epitope(s), which interact with vitronectin (VN), integrins, and caveolin, thus modifying the substrate specificity. Thus, u-PA binding can transform u-PAR from a simple receptor for u-PA into a pleiotropic ligand for other surface molecules.All of these processes are regulated by the u-PA inhibitor, PAI-1. Inhibition of cell adhesion and migration by PAI-1 on VN occurs because the same region of VN is required for interaction with PAI-1, u-PAR, and integrins. PAI-1, however, also affects u-PAR occupancy by triggering the internalization of the u-PA-u-PAR complex, the degradation of u-PA, and the recycling of free u-PAR. Available data suggest that cells respond to a “stop” signal, due to the PAI-1-dependent internalization and degradation of u-PA. Cells also respond to a “go” signal through the stimulation of surface-proteolysis, exposure of chemotactic epitopes, and recycling of u-PAR to novel surface positions. Finally, cells respond to a “pause” signal through transient u-PAR-dependent adhesion stages, thus shifting the cells between an “adhesion-mode” and a “migration-mode.”

scholarly journals ANGPTL4 overexpression inhibits tumor cell adhesion and migration and predicts favorable prognosis of triple-negative breast cancer

BMC Cancer ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Yu-Chen Cai ◽  
Hang Yang ◽  
Ke-Feng Wang ◽  
Tan-Huan Chen ◽  
Wen-Qi Jiang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Migration And Invasion ◽  
Tumor Cell Adhesion ◽  
Tumor Tissues ◽  
Cell Adhesion And Migration ◽  
And Migration

Abstract Background Triple-negative breast cancer (TNBC) patients have relatively poor clinical outcomes. A marker predicting the prognosis of patients with TNBC could help guide treatment. Extensive evidence demonstrates that angiopoietin-like 4 (ANGPTL4) is involved in the regulation of cancer growth, metastasis and angiogenesis. Therefore, its role in TNBC is of interest. Methods: We tested the ANGPTL4 expression level in tumor tissues by immunohistochemistry (IHC) and detected its association with the clinical features of TNBC patients. Next, the effects and mechanisms of ANGPTL4 on TNBC cell migration and adhesion were investigated. Results We found that ANGPTL4 overexpression was associated with favorable outcomes in TNBC patients. ANGPTL4 upregulation inhibited cell adhesion, migration and invasion in vitro. Further analyses demonstrated that the possible mechanism might involve suppression of TNBC progression by interacting with extracellular matrix-related genes. Conclusions The present findings demonstrated that enhancement of ANGPTL4 expression might inversely correlate with TNBC progression. ANGPTL4 is a promising marker of TNBC and should be evaluated in further studies. Trial registration Retrospectively registered.

Sign in / Sign up

Export Citation Format

Share Document