Aggregation of Burkitt Lymphoma Cells in Stationary Culture: Experimental and Theoretical Analysis

1972 ◽  
Vol 10 (3) ◽  
pp. 749-758
Author(s):  
E. MAYHEW ◽  
L. E. BLUMENSON
Keyword(s):  
Computer Simulation ◽  
Cell Motility ◽  
Burkitt Lymphoma ◽  
Cell Movement ◽  
Experimental System ◽  
Cell Aggregation ◽  
Cellular Motility ◽  
Final Size ◽  
Lymphoma Cells ◽  
Aggregation Behaviour

Cellular motility plays an important role in natural aggregative phenomena but previously has been difficult to quantitate. We here describe a general method which can be used to determine the importance of cell motility in cell aggregation behaviour. When actively moving Burkitt lymphoma cells cultured in microtest plate wells come into contact they adhere to one another forming an aggregate. The aggregate increases in size when more cells come in contact with it. The final size and number of aggregates per well was found to be dependent on the number of cells added per well. With increasing cell numbers added per well the number of aggregates formed increased until it reached a peak of 47-57 aggregates per well 20 h after the addition of 180-710 cells per well. At higher cell concentrations the number of aggregates formed decreased. The system was analysed theoretically by programming a computer to simulate the experimental system. This simulation showed it was probable that the experimental results obtained were due to (a) random dropping of the cells at zero time and (b) the adhesion of the cells when they made contact and (c) unrestricted random movement of cells in the well when they reached the well surface. The computer simulation is such that given the experimentally determined cell concentration per well and rate of cell movement we can predict the number of aggregates formed for different probabilities that the adhesions formed after the cells come in contact are permanent. This experimental approach along with the computer simulation can be used to quantitate the role of cell motility and permanence of contact in cell aggregation.

scholarly journals Actinin-4, a Novel Actin-bundling Protein Associated with Cell Motility and Cancer Invasion

1998 ◽  
Vol 140 (6) ◽  
pp. 1383-1393 ◽  
Author(s):  
Kazufumi Honda ◽  
Tesshi Yamada ◽  
Ritsuko Endo ◽  
Yoshinori Ino ◽  
Masahiro Gotoh ◽  
...  
Keyword(s):  
Actin Cytoskeleton ◽  
Cell Motility ◽  
Cell Movement ◽  
Metastatic Potential ◽  
Cancer Invasion ◽  
Cytoplasmic Localization ◽  
Cellular Motility ◽  
Phosphatidylinositol 3 Kinase ◽  
Antigenic Protein ◽  
Histological Phenotype

Regulation of the actin cytoskeleton may play a crucial role in cell motility and cancer invasion. We have produced a monoclonal antibody (NCC- Lu-632, IgM, k) reactive with an antigenic protein that is upregulated upon enhanced cell movement. The cDNA for the antigen molecule was found to encode a novel isoform of nonmuscle α-actinin. This isoform (designated actinin-4) was concentrated in the cytoplasm where cells were sharply extended and in cells migrating and located at the edge of cell clusters, but was absent from focal adhesion plaques or adherens junctions, where the classic isoform (actinin-1) was concentrated. Actinin-4 shifted steadily from the cytoplasm to the nucleus upon inhibition of phosphatidylinositol 3 kinase or actin depolymerization. The cytoplasmic localization of actinin-4 was closely associated with an infiltrative histological phenotype and correlated significantly with a poorer prognosis in 61 cases of breast cancer. These findings suggest that cytoplasmic actinin-4 regulates the actin cytoskeleton and increases cellular motility and that its inactivation by transfer to the nucleus abolishes the metastatic potential of human cancers.

scholarly journals Neuropeptide Y/Y5 Receptor Pathway Stimulates Neuroblastoma Cell Motility Through RhoA Activation

2021 ◽  
Vol 8 ◽  
Author(s):  
Nouran Abualsaud ◽  
Lindsay Caprio ◽  
Susana Galli ◽  
Ewa Krawczyk ◽  
Lamia Alamri ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Cell Motility ◽  
Neuroblastoma Cell ◽  
Cell Movement ◽  
Cellular Motility ◽  
Rhoa Activity ◽  
Rhoa Activation ◽  
Cytoskeleton Remodeling ◽  
Cancer Dissemination ◽  
Migratory Cells

Neuropeptide Y (NPY) has been implicated in the regulation of cellular motility under various physiological and pathological conditions, including cancer dissemination. Yet, the exact signaling pathways leading to these effects remain unknown. In a pediatric malignancy, neuroblastoma (NB), high NPY release from tumor tissue associates with metastatic disease. Here, we have shown that NPY stimulates NB cell motility and invasiveness and acts as a chemotactic factor for NB cells. We have also identified the Y5 receptor (Y5R) as the main NPY receptor mediating these actions. In NB tissues and cell cultures, Y5R is highly expressed in migratory cells and accumulates in regions of high RhoA activity and dynamic cytoskeleton remodeling. Y5R stimulation activates RhoA and results in Y5R/RhoA-GTP interactions, as shown by pull-down and proximity ligation assays, respectively. This is the first demonstration of the role for the NPY/Y5R axis in RhoA activation and the subsequent cytoskeleton remodeling facilitating cell movement. These findings implicate Y5R as a target in anti-metastatic therapies for NB and other cancers expressing this receptor.

scholarly journals 2D or 3D? How in vitro cell motility is conserved across dimensions, and predicts in vivo invasion

2019 ◽  
Author(s):  
Sualyneth Galarza ◽  
Hyuna Kim ◽  
Naciye Atay ◽  
Shelly R Peyton ◽  
Jennifer M Munson
Keyword(s):  
Cell Migration ◽  
Cell Motility ◽  
Cell Movement ◽  
Complex Model ◽  
Model Systems ◽  
Cellular Motility ◽  
Statistical Tool ◽  
3D Environments

AbstractCell motility is a critical aspect of wound healing, the immune response, and is deregulated in cancer. Current limitations in imaging tools make it difficult to study cell migration in vivo. To overcome this, and to identify drivers from the microenvironment that regulate cell migration, bioengineers have developed 2D and 3D tissue model systems in which to study cell motility in vitro, with the aim of mimicking the environments in which cells move in vivo. However, there has been no systematic study to explicitly relate and compare cell motility measurements between these geometries/systems. Here, we provide such analysis on our own data, as well as across data in existing literature to understand whether, and which, in vitro models are predictive of in vivo cell motility. To our surprise, many metrics of cell movement on 2D surfaces significantly and positively correlate with cell migration in 3D environments, and cell invasion in 3D is negatively correlated with glioblastoma invasion in vivo. Finally, to best compare across complex model systems, in vivo data, and data from different labs, we suggest that groups report an effect size, a statistical tool that is most translatable across experiments and labs, when conducting experiments that affect cellular motility.

Selective serotonin reuptake inhibitors directly signal for apoptosis in biopsy-like Burkitt lymphoma cells

Blood ◽  
2003 ◽  
Vol 101 (8) ◽  
pp. 3212-3219 ◽  
Author(s):  
Adamantios Serafeim ◽  
Michelle J. Holder ◽  
Gillian Grafton ◽  
Anita Chamba ◽  
Mark T. Drayson ◽  
...  
Keyword(s):  
Burkitt Lymphoma ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Mononuclear Cells ◽  
Serotonin Reuptake Inhibitors ◽  
Calcium Flux ◽  
Selective Serotonin ◽  
Future Application ◽  
Lymphoma Cells ◽  
Normal Peripheral Blood

Abstract Selective serotonin reuptake inhibitors (SSRIs) are the treatment of choice for clinical depression and a range of anxiety-related disorders. They are well tolerated over extended periods with more than 50 million people worldwide benefiting from their use. Here we show that 3 structurally distinct SSRIs—fluoxetine, paroxetine, and citalopram—act directly on Burkitt lymphoma (BL) cells to trigger rapid and extensive programmed cell death. SSRIs unexpectedly stimulated calcium flux, tyrosine phosphorylation, and down-regulation of the c-myc and nm23 genes in Burkitt lymphoma cells remaining faithful to the biopsy phenotype. Resultant SSRI-induced apoptosis was preceded by caspase activation, poly(ADP-ribose) polymerase-1 (PARP-1) cleavage, DNA fragmentation, a loss of mitochondrial membrane potential, and the externalization of phosphatidylserine, and reversed by the overexpression of bcl-2. Normal peripheral blood mononuclear cells and tonsil B cells, whether resting or stimulated into cycle, were largely resistant to SSRI-induced death as were 5 non-BL lymphoid cell lines tested. We discuss these findings within the context of whether the SSRI class of antidepressants could find future application as potential therapeutics for the highly aggressive and—because of its association with AIDS—increasingly more common Burkitt lymphoma.

scholarly journals Modulation of Cellular Migration and Survival by c-Myc through the Downregulation of Urokinase (uPA) and uPA Receptor

2010 ◽  
Vol 30 (7) ◽  
pp. 1838-1851 ◽  
Author(s):  
Daniela Alfano ◽  
Giuseppina Votta ◽  
Almut Schulze ◽  
Julian Downward ◽  
Mario Caputi ◽  
...  
Keyword(s):  
Cell Motility ◽  
Cellular Transformation ◽  
Tumor Formation ◽  
Cellular Migration ◽  
Epithelial Cell Line ◽  
Cellular Motility ◽  
Upa Receptor ◽  
Upar Expression ◽  
Repressive Effect ◽  
Cell Invasiveness

ABSTRACT It has been proposed that c-Myc proapoptotic activity accounts for most of its restraint of tumor formation. We established a telomerase-immortalized human epithelial cell line expressing an activatable c-Myc protein. We found that c-Myc activation induces, in addition to increased sensitivity to apoptosis, reductions in cell motility and invasiveness. Transcriptome analysis revealed that urokinase (uPA) and uPA receptor (uPAR) were strongly downregulated by c-Myc. Evidence is provided that the repression of uPA and uPAR may account for most of the antimigratory and proapoptotic activities of c-Myc. c-Myc is known to cooperate with Ras in cellular transformation. We therefore investigated if this cooperation could converge in the control of uPA/uPAR expression. We found that Ras is able to block the effects of c-Myc activation on apoptosis and cellular motility but not on cell invasiveness. Accordingly, the activation of c-Myc in the context of Ras expression had only minor influence on uPAR expression but still had a profound repressive effect on uPA expression. Thus, the differential regulation of uPA and uPAR by c-Myc and Ras correlates with the effects of these two oncoproteins on cell motility, invasiveness, and survival. In conclusion, we have discovered a novel link between c-Myc and uPA/uPAR. We propose that reductions of cell motility and invasiveness could contribute to the inhibition of tumorigenesis by c-Myc and that the regulation of uPA and uPAR expression may be a component of the ability of c-Myc to reduce motility and invasiveness.

Effects of Cytochalasins on the Initial Aggregation in Vitro of Embryonic Chick Cells

1974 ◽  
Vol 14 (1) ◽  
pp. 187-196
Author(s):  
J. C. APPLETON ◽  
R. B. KEMP
Keyword(s):  
Cytochalasin B ◽  
Cell Aggregation ◽  
Cellular Injury ◽  
Cellular Motility ◽  
Carbon Dioxide Evolution ◽  
Site Of Action ◽  
Dissociated Cells ◽  
Cytochalasin A ◽  
Final Confirmation

The initial aggregation of trypsin-dissociated cells from the skeletal muscle tissue of 9-day-old chick embryos in the presence of cytochalasins A and B was studied in order to discover the effects of these agents on contact and adhesion. Cytochalasin B (3 µg/ml) had a negligible effect on the rate of aggregation of cells over an 8-h period, but cytochalasin A at concentrations between 3 and 20 µg/ml markedly inhibited aggregation. Both agents altered the shape and size of aggregates and caused cells at their periphery to appear more spherical. The oxygen uptake of the treated cells was not noticeably different from that of the controls, despite the severe inhibition of isotopic carbon dioxide evolution. The effect of cytochalasin B on cell aggregation was reversible and although the cytochalasin A effect could not be abolished on return to medium free of A, the unaltered oxygen consumption was taken as an indication that permanent cellular injury did not occur. The effect of the cytochalasins on aggregate structure was interpreted on the basis of arrested cellular motility, but the singular inhibition by cytochalasin A of the rate of aggregation must await final confirmation of its site of action.

Effect of centrifugation on the viability of Burkitt lymphoma cells

1968 ◽  
Vol 10 (5) ◽  
pp. 641-649 ◽  
Author(s):  
Daniel I. C. Wang ◽  
Tony J. Sinskey ◽  
Robert E. Gerner ◽  
Richard P. De Filippi
Keyword(s):  
Burkitt Lymphoma ◽  
Lymphoma Cells

scholarly journals Synchrony of Burkitt Lymphoma Cells Induced by Hydroxyurea

1976 ◽  
Vol 1 (2) ◽  
pp. 177-185
Author(s):  
Tadaaki Miyamoto ◽  
Michinori Watanabe ◽  
Yosinobu Takabe ◽  
Toyozo Terasima
Keyword(s):  
Burkitt Lymphoma ◽  
Lymphoma Cells
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