Analysis of the number of size parameters that can be reliably estimated from cell scattering

2021 ◽  
Author(s):  
Ashley E. Cannaday ◽  
Rajdeep Singh ◽  
James Hoelle
Keyword(s):  
Cell Scattering

Computational analysis of mitochondrial placement and aggregation effects on wide-angle cell scattering patterns

2009 ◽  
Author(s):  
Patrick M. Pilarski ◽  
Xuan-Tao Su ◽  
D. Moira Glerum ◽  
Christopher J. Backhouse
Keyword(s):  
Computational Analysis ◽  
Wide Angle ◽  
Cell Scattering

Ras induces NBT-II epithelial cell scattering through the coordinate activities of Rac and MAPK pathways

2002 ◽  
Vol 115 (12) ◽  
pp. 2591-2601 ◽  
Author(s):  
Natacha Edme ◽  
Julian Downward ◽  
Jean-Paul Thiery ◽  
Brigitte Boyer
Keyword(s):  
Cell Migration ◽  
Cell Motility ◽  
Mapk Pathway ◽  
Small Gtpase ◽  
Dominant Negative Mutant ◽  
Cell Periphery ◽  
Cell Dissociation ◽  
Downstream Targets ◽  
Cell Dispersion ◽  
Cell Scattering

Cell dissociation and cell migration are the two main components of epithelium-mesenchyme transitions (EMT). We previously demonstrated that Ras is required for the accomplishment of both of these processes during the EGF-induced EMT of the NBT-II rat carcinoma cell line in vitro. In this study,we examined the downstream targets of Ras that are responsible for the dissociation and motility of NBT-II cells. Overexpression of activated forms of c-Raf and MEK1 (a component of the mitogen-activated protein kinase pathway, MAPK) led to cell dissociation, as inferred by the loss of desmosomes from the cell periphery. By contrast, active PI3K, RalA and RalB did not induce desmosome breakdown. The MEK1 inhibitor PD098059 inhibited EGF- and Ras-induced cell dispersion, whereas the PI3K inhibitor LY294002 had no effect. Accordingly, among the partial loss-of-function mutants of Ras(RasV12) that were used to distinguish between downstream targets of Ras, we found that the Raf-specific Ras mutants RasV12S35 and RasV12E38 induced cell dissociation. The PI3K- and RalGDS-activating Ras mutants had, in contrast, no effect on cell dispersion. However, MEK1 was unable to promote cell motility,whereas RasV12S35 and RasV12E38 induced cell migration, suggesting that another Ras effector was responsible for cell motility. We found that the small GTPase Rac is necessary for EGF-mediated cell dispersion since overexpression of a dominant-negative mutant of Rac1 (Rac1N17) inhibited EGF-induced NBT-II cell migration. All stimuli that promoted cell migration also induced Rac activation. Finally, coexpression of active Rac1 and active MEK1 induced the motility of NBT-II cells, suggesting that Ras mediates NBT-II cell scattering through the coordinate activation of Rac and the Raf/MAPK pathway.

scholarly journals Enhancement of Hepatocyte Growth Factor-Induced Cell Scattering in N-Acetylglucosaminyltransferase III-transfected HepG2 Cells

2004 ◽  
Vol 27 (6) ◽  
pp. 781-785 ◽  
Author(s):  
Masashi Hyuga ◽  
Sumiko Hyuga ◽  
Nana Kawasaki ◽  
Miyako Ohta ◽  
Satsuki Itoh ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Hepg2 Cells ◽  
Cell Scattering ◽  
Hepatocyte Growth

scholarly journals Spatial recruitment and activation of the Fes kinase by ezrin promotes HGF-induced cell scattering

2007 ◽  
Vol 27 (1) ◽  
pp. 38-50 ◽  
Author(s):  
Alexandra Naba ◽  
Céline Reverdy ◽  
Daniel Louvard ◽  
Monique Arpin
Keyword(s):  
Cell Scattering

Rho family GTPases are activated during HGF-stimulated prostate cancer-cell scattering

2005 ◽  
Vol 62 (3) ◽  
pp. 180-194 ◽  
Author(s):  
C. M. Wells ◽  
T. Ahmed ◽  
J. R. W. Masters ◽  
G. E. Jones
Keyword(s):  
Prostate Cancer ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Rho Family Gtpases ◽  
Cell Scattering ◽  
Rho Family

scholarly journals pp60c-src is a positive regulator of growth factor-induced cell scattering in a rat bladder carcinoma cell line.

1995 ◽  
Vol 131 (3) ◽  
pp. 761-773 ◽  
Author(s):  
J M Rodier ◽  
A M Vallés ◽  
M Denoyelle ◽  
J P Thiery ◽  
B Boyer
Keyword(s):  
Growth Factor ◽  
Signaling Pathways ◽  
Cell Line ◽  
Intracellular Signaling ◽  
Carcinoma Cell ◽  
Biological Activities ◽  
Dominant Negative ◽  
Carcinoma Cell Line ◽  
Dominant Negative Mutant ◽  
Cell Scattering

The NBT-II rat carcinoma cell line exhibits two mutually exclusive responses to FGF-1 and EGF, entering mitosis at cell confluency while undergoing an epithelium-to-mesenchyme transition (EMT) when cultured at subconfluency. EMT is characterized by acquisition of cell motility, modifications of cell morphology, and cell dissociation correlating with the loss of desmosomes from cellular cortex. The pleiotropic effects of EGF and FGF-1 on NBT-II cells suggest that multiple signaling pathways may be activated. We demonstrate here that growth factor activation is linked to at least two intracellular signaling pathways. One pathway leading to EMT involves an early and sustained stimulation of pp60c-src kinase activity, which is not observed during the growth factor-induced entry into the cell cycle. Overexpression of normal c-src causes a subpopulation of cells to undergo spontaneous EMT and sensitizes the rest of the population to the scattering activity of EGF and FGF-1 without affecting their mitogenic responsiveness. Addition of cholera toxin, a cAMP-elevating agent, severely perturbs growth factor induction of EMT without altering pp60c-src activation, therefore demonstrating that cAMP blockade takes place downstream or independently of pp60c-src. On the other hand, overexpression of a mutated, constitutively activated form of pp60c-src does not block cell dispersion while strongly inhibiting growth factor-induced entry into cell division. Moreover, stable transfection of a dominant negative mutant of c-src inhibits the scattering response without affecting mitogenesis induced by the growth factors. Altogether, these results suggest a role for pp60c-src in epithelial cell scattering and indicate that pp60c-src might contribute unequally to the two separate biological activities engendered by a single signal.

scholarly journals Modulation of Rac1 and ARF6 Activation during Epithelial Cell Scattering

2003 ◽  
Vol 278 (19) ◽  
pp. 17395-17400 ◽  
Author(s):  
Felipe Palacios ◽  
Crislyn D'Souza-Schorey
Keyword(s):  
Epithelial Cell ◽  
Cell Scattering
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