scholarly journals Modulation of tumor cell migration, invasion and cell-matrix adhesion by human monopolar spindle-one-binder 2

2015 ◽  
Vol 33 (5) ◽  
pp. 2495-2503 ◽  
Author(s):  
WENJUAN WU ◽  
XIZHI ZHANG ◽  
HAONAN QIN ◽  
WANXIN PENG ◽  
QINGYU XUE ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumor Cell ◽  
Tumor Cell Migration ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Monopolar Spindle ◽  
Cell Matrix Adhesion

Cell–matrix adhesion complexes: Master control machinery of cell migration

2008 ◽  
Vol 18 (1) ◽  
pp. 65-76 ◽  
Author(s):  
John G. Lock ◽  
Bernhard Wehrle-Haller ◽  
Staffan Strömblad
Keyword(s):  
Cell Migration ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion ◽  
Master Control

scholarly journals The protein-tyrosine phosphatase DEP-1 modulates growth factor-stimulated cell migration and cell–matrix adhesion

Oncogene ◽  
2003 ◽  
Vol 22 (27) ◽  
pp. 4175-4185 ◽  
Author(s):  
Enrico Jandt ◽  
Karsten Denner ◽  
Marina Kovalenko ◽  
Arne Östman ◽  
Frank-D Böhmer
Keyword(s):  
Cell Migration ◽  
Growth Factor ◽  
Protein Tyrosine Phosphatase ◽  
Tyrosine Phosphatase ◽  
Protein Tyrosine ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion

scholarly journals RAP1-RAC1 Signaling Has an Important Role in Adhesion and Migration in HNSCC

2020 ◽  
Vol 99 (8) ◽  
pp. 959-968 ◽  
Author(s):  
M. Liu ◽  
R. Banerjee ◽  
C. Rossa ◽  
N.J. D’Silva
Keyword(s):  
Cell Migration ◽  
Cell Adhesion ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
And Migration ◽  
Rap1 Activation ◽  
Cell Matrix Adhesion ◽  
Α5β1 Integrin ◽  
Hnscc Cell ◽  
Cell Cell

Cell-cell adhesion is a key mechanism to control tissue integrity and migration. In head and neck squamous cell carcinoma (HNSCC), cell migration facilitates distant metastases and is correlated with poor prognosis. RAP1, a ras-like protein, has an important role in the progression of HNSCC. RAC1 is an integrin-linked, ras-like protein that promotes cell migration. Here we show that loss of cell-cell adhesion is correlated with inactivation of RAP1 confirmed by 2 different biochemical approaches. RAP1 activation is required for cell-matrix adhesion confirmed by adhesion to fibronectin-coated plates with cells that have biochemically activated RAP1. This effect is reversed when RAP1 is inactivated. In addition, RAP1GTP-mediated adhesion is only facilitated through α5β1 integrin complex and is not a function of either α5 or β1 integrin alone. Moreover, the inside-out signaling of RAP1 activation is coordinated with RAC1 activation. These findings show that RAP1 has a prominent role in cell-matrix adhesion via extracellular matrix molecule fibronectin-induced α5β1 integrin and supports a critical role for the RAP1/RAC1 signaling axis in HNSCC cell migration.

scholarly journals Increased Cell-Matrix Adhesion upon Constitutive Activation of Rho Proteins by Cytotoxic Necrotizing Factors from E. coli and Y. pseudotuberculosis

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Martin May ◽  
Tanja Kolbe ◽  
Tianbang Wang ◽  
Gudula Schmidt ◽  
Harald Genth
Keyword(s):  
Cell Migration ◽  
Hela Cells ◽  
Adherent Cells ◽  
Rho Proteins ◽  
E Coli ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Established Cell ◽  
Cell Matrix Adhesion ◽  
Suspended Cells

Cytotoxic necrotizing factors (CNFs) encompass a class of autotransporter toxins produced by uropathogenic E. coli (CNF1) or Y. pseudotuberculosis (CNFy). CNF toxins deamidate and thereby constitutively activate RhoA, Rac1, and Cdc42. In this study, the effects of CNF1 on cell-matrix adhesion are analysed using functional cell-adhesion assays. CNF1 strongly increased cell-matrix binding of suspended Hela cells and decreased the susceptibly of cells to trypsin-induced cell detachment. Increased cell-matrix binding was also observed upon treatment of Hela cells with isomeric CNFy, that specifically deamidates RhoA. Increased cell-matrix binding thus appears to depend on RhoA deamidation. In contrast, increased cell spreading was specifically observed upon CNF1 treatment, suggesting that it rather depended on Rac1/Cdc42 deamidation. Increased cell-matrix adhesion is further presented to result in reduced cell migration of adherent cells. In contrast, migration of suspended cells was not affected upon treatment with CNF1 or CNFy. CNF1 and CNFy thus reduced cell migration specifically under the condition of pre-established cell-matrix adhesion.

scholarly journals CASP4 gene silencing in epithelial cancer cells leads to impairment of cell migration, cell-matrix adhesion and tissue invasion

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Giuliana Papoff ◽  
Dario Presutti ◽  
Cristiana Lalli ◽  
Giulia Bolasco ◽  
Simonetta Santini ◽  
...  
Keyword(s):  
Cell Migration ◽  
Gene Silencing ◽  
Cancer Cells ◽  
Epithelial Cancer ◽  
Tissue Invasion ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion

scholarly journals Spatial heterogeneity of cell-matrix adhesive forces predicts human glioblastoma migration

2020 ◽  
Author(s):  
Rasha Rezk ◽  
Bill Zong Jia ◽  
Astrid Wendler ◽  
Ivan Dimov ◽  
Colin Watts ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Lines ◽  
Adhesion Strength ◽  
Fluorescence Intensity ◽  
Sampling Location ◽  
Adhesion Properties ◽  
Tumor Mass ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion

AbstractBackgroundGlioblastoma (GBM) is a highly aggressive incurable brain tumor. The main cause of mortality in GBM patients is the invasive rim of cells migrating away from the main tumor mass and invading healthy parts of the brain. Although motion is driven by forces, our current understanding of the physical factors involved in glioma infiltration remains limited. This study aims to investigate the adhesion properties within and between patients’ tumors on a cellular level and test whether these properties correlate with cell migration.MethodsNine tissue samples were taken from spatially separated sections during 5-aminolevulinic acid (5-ALA) fluorescence guided surgery. Navigated biopsy samples were collected from strongly fluorescent tumor cores, a weak fluorescent tumor rim, and non-fluorescent tumor margins. A microfluidics device was built to induce controlled shear forces to detach cells from monolayer cultures. Cells were cultured on low modulus polydimethylsiloxane representative of the stiffness of brain tissue. Cell migration and morphology were then obtained using time lapse microscopy.ResultsGBM cell populations from different tumor fractions of the same patient exhibited different migratory and adhesive behaviors. These differences were associated with sampling location and amount of 5-ALA fluorescence. Cells derived from weak- and non-fluorescent tumor tissue were smaller, adhered less well, and migrated quicker than cells derived from strongly fluorescent tumor mass.ConclusionGBM tumors are biomechanically heterogeneous. Selecting multiple populations and broad location sampling are therefore important to consider for drug testing.Key pointsGBM tumors are biomechanically heterogeneousGBM cell migration is inversely correlated with cell-matrix adhesion strength5-ALA fluorescence intensity during surgery correlates with the motility properties of GBM cellsImportance of the studyThis is the first study to compare single cell migration and cell-matrix adhesion strength of GBM, using cell lines derived from different tumors and from different regions within the same tumor. Not accounting for internal sampling location within each tumor obscures differences in cell morphology, motility and adhesion properties between patients. Peripherical and marginal tumor cells have different adhesion profiles and are highly migratory compared to those found in the core of the tumor. Aggressive regions of the tumor (highly motile) are linked to the spatial distribution of adhesion strength and are strongly associated with 5-ALA fluorescence intensity. Preclinical tests aimed at developing a treatment for GBM using anti-invasive drugs or adhesion inhibitors, would benefit from using cell lines derived from the tumor periphery (with low 5-ALA intensity) rather than cell lines derived from the tumor core.

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