αvβ3 integrin engagement modulates cell adhesion, proliferation, and protease secretion in human lymphoid tumor cells

2001 ◽  
Vol 29 (8) ◽  
pp. 993-1003 ◽  
Author(s):  
A Vacca
Keyword(s):  
Cell Adhesion ◽  
Tumor Cells ◽  
Αvβ3 Integrin ◽  
Lymphoid Tumor ◽  
Protease Secretion

scholarly journals EXPRESSION OF NEURAL CELL ADHESION MOLECULES IN THE MOUSE ANTERIOR PITUITARY GLAND AND PITUITARY TUMOR CELLS

1998 ◽  
Vol 19 (4) ◽  
pp. 269-277
Author(s):  
YOSHIHIRO YAYOI ◽  
SUMIO TAKAHASHI ◽  
SAKAE TAKEUCHI ◽  
MAKOTO TAKEUCHI ◽  
TATSUNORI SEKI ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Pituitary Gland ◽  
Tumor Cells ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Pituitary Tumor ◽  
Anterior Pituitary ◽  
Neural Cell ◽  
Neural Cell Adhesion Molecules ◽  
Neural Cell Adhesion

scholarly journals Nanostructured Surfaces to Target and Kill Circulating Tumor Cells While Repelling Leukocytes

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Michael J. Mitchell ◽  
Carlos A. Castellanos ◽  
Michael R. King
Keyword(s):  
Cell Adhesion ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Cancer Cell ◽  
Halloysite Nanotubes ◽  
Breast Adenocarcinoma ◽  
Hematogenous Metastasis ◽  
Mcf7 Cells ◽  
Nanostructured Surfaces ◽  
Cancer Cell Death

Hematogenous metastasis, the process of cancer cell migration from a primary to distal location via the bloodstream, typically leads to a poor patient prognosis. Selectin proteins hold promise in delivering drug-containing nanocarriers to circulating tumor cells (CTCs) in the bloodstream, due to their rapid, force-dependent binding kinetics. However, it is challenging to deliver such nanocarriers while avoiding toxic effects on healthy blood cells, as many possess ligands that adhesively interact with selectins. Herein, we describe a nanostructured surface to capture flowing cancer cells, while preventing human neutrophil adhesion. Microtube surfaces with immobilized halloysite nanotubes (HNTs) and E-selectin functionalized liposomal doxorubicin (ES-PEG L-DXR) significantly increased the number of breast adenocarcinoma MCF7 cells captured from flow, yet also significantly reduced the number of captured neutrophils. Neutrophils firmly adhered and projected pseudopods on surfaces coated only with liposomes, while neutrophils adherent to HNT-liposome surfaces maintained a round morphology. Perfusion of both MCF7 cells and neutrophils resulted in primarily cancer cell adhesion to the HNT-liposome surface, and induced significant cancer cell death. This work demonstrates that nanostructured surfaces consisting of HNTs and ES-PEG L-DXR can increase CTC recruitment for chemotherapeutic delivery, while also preventing healthy cell adhesion and uptake of therapeutic intended for CTCs.

Reduced expression of plakoglobin indicates an unfavorable prognosis in subsets of patients with non-small-cell lung cancer.

1998 ◽  
Vol 16 (4) ◽  
pp. 1407-1413 ◽  
Author(s):  
K Pantel ◽  
B Passlick ◽  
J Vogt ◽  
P Stosiek ◽  
M Angstwurm ◽  
...  
Keyword(s):  
Risk Factors ◽  
Lung Cancer ◽  
Overall Survival ◽  
Cell Adhesion ◽  
Lymph Node ◽  
Tumor Cells ◽  
Primary Tumor ◽  
Small Cell ◽  
Small Cell Lung ◽  
Disease Free

PURPOSE Plakoglobin is thought to play a key role in cadherin-mediated epithelial cell adhesion, because it is a common component of desmosomal and nondesmosomal adherens junctions. Because loss of homotypic cell adhesion is an important early step in invasion and metastasis of solid tumors, we evaluated the frequency and prognostic significance of a deficient expression of plakoglobin in human lung cancer. PATIENTS AND METHODS At primary surgery, representative specimens of the primary tumor were obtained from 96 consecutive patients with completely resected non-small-cell lung carcinoma (NSCLC) without overt distant metastases. Cryostat sections of these specimens and metastatic lymph nodes were stained with monoclonal antibody (mAb) PG 5.1 against plakoglobin, using an immunoperoxidase technique. Patients were monitored for a median of 39 months (range, 12 to 56) after surgery. RESULTS Absent or severely reduced expression of plakoglobin (ie, < 30% positive tumor cells) was observed in 39 patients (40.6%). There was no significant correlation to established risk factors, such as the histology, extension, and histologic grade of the primary tumor and metastatic lymph node involvement, or expression of alpha-catenin. Expression of plakoglobin in lymph node metastases ranged from 0% to greater than 60% positive tumor cells. Deficient plakoglobin expression on the primary tumor was significantly correlated to a shortened disease-free and overall survival in patients with adenocarcinomas, pT1-2 tumors, or negative lymph nodes (pN0). In patients with pT1-2 tumors, the independence of this prognostic influence from established risk factors was demonstrated by Cox regression analyses (disease-free survival, P = .002; overall survival, P = .038). CONCLUSION Deficient expression of plakoglobin appears to be an important event in the progression of NSCLC.

Neutrophils Rolling on Immobilised Platelets Migrate into Homotypic Aggregates after Activation

1998 ◽  
Vol 79 (06) ◽  
pp. 1177-1183 ◽  
Author(s):  
Christopher Buckley ◽  
David Simmons ◽  
Gerard Nash ◽  
G. E. Rainger
Keyword(s):  
Cell Adhesion ◽  
Vascular Disease ◽  
Adhesion Molecules ◽  
Platelet Activating Factor ◽  
Vascular Occlusion ◽  
Adhesion Assay ◽  
Αvβ3 Integrin ◽  
Projected Area ◽  
Activated Platelets ◽  
Cell Cell

SummaryInteractions between platelets and leucocytes are implicated in the pathology of thrombotic vascular disease. Using a flow-based adhesion assay we have investigated a novel route for the formation of neutrophil aggregates on the surface of immobilised activated platelets. Neutrophils perfused over a platelet monolayer formed numerous rolling attachments but rapidly stopped and spread after the superfusion of N-formyl-methionyl-leucyl-phenylalanine or platelet-activating factor (both at 10–7 M). Subsequent integrin-mediated migration across the platelet monolayer enabled formation of homotypic neutrophil aggregates, which was significant within 2.5 min of receipt of either stimulus. Aggregates increased in size with time and had an average projected area of ~500 μm2 after 10 min. Increasing size was correlated with an increasing tendency for movement downstream and large aggregates sometimes tumbled in that direction. The formation and stability of homotypic aggregates was dependent on several adhesive mechanisms. Antibody blockade demonstrated that interactions involving CD11a/ CD18 and ICAM-3, between αvβ3-integrin and CD31 and between L-selectin and an unidentified counter-ligand were all required for the complete aggregatory response. Furthermore, blockade of L-selectin allowed initial aggregation which then reversed, suggesting that this receptor might regulate the interactions between other adhesion molecules that directly supported cell-cell adhesion. We propose that this novel route for leucocyte aggregation could promote vascular occlusion in thrombotic vessels or at distal sites in the event of embolisation.

scholarly journals The fibronectin synergy site re-enforces cell adhesion and mediates a crosstalk between integrin classes

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Maria Benito-Jardón ◽  
Sarah Klapproth ◽  
Irene Gimeno-LLuch ◽  
Tobias Petzold ◽  
Mitasha Bharadwaj ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Thrombus Formation ◽  
Critical Role ◽  
Initial Contact ◽  
Αvβ3 Integrin ◽  
Rgd Motif ◽  
Cell Coverage ◽  
Vessel Injury ◽  
Close Proximity ◽  
External Forces

Fibronectin (FN), a major extracellular matrix component, enables integrin-mediated cell adhesion via binding of α5β1, αIIbβ3 and αv-class integrins to an RGD-motif. An additional linkage for α5 and αIIb is the synergy site located in close proximity to the RGD motif. We report that mice with a dysfunctional FN-synergy motif (Fn1syn/syn) suffer from surprisingly mild platelet adhesion and bleeding defects due to delayed thrombus formation after vessel injury. Additional loss of β3 integrins dramatically aggravates the bleedings and severely compromises smooth muscle cell coverage of the vasculature leading to embryonic lethality. Cell-based studies revealed that the synergy site is dispensable for the initial contact of α5β1 with the RGD, but essential to re-enforce the binding of α5β1/αIIbβ3 to FN. Our findings demonstrate a critical role for the FN synergy site when external forces exceed a certain threshold or when αvβ3 integrin levels decrease below a critical level.

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