Cell Motility in Tumor Invasion

2002 ◽  
Author(s):  
Alan Wells ◽  
Douglas A. Lauffenburger ◽  
Timothy Turner
Keyword(s):  
Cell Motility ◽  
Tumor Invasion

The role of E-cadherin and scatter factor in tumor invasion and cell motility

1991 ◽  
pp. 109-126 ◽  
Author(s):  
Jürgen Behrens ◽  
K. Michael Weidner ◽  
Uwe H. Frixen ◽  
Jörg H. Schipper ◽  
Martin Sachs ◽  
...  
Keyword(s):  
Cell Motility ◽  
Tumor Invasion ◽  
Scatter Factor ◽  
E Cadherin

scholarly journals Downregulation of Src Family Kinase Activity Using PP2 Inhibitor Has No Effect on the Elongation of Pragmin-Transfected Adenocarcinoma AGS cells

2018 ◽  
Vol 3 (1) ◽  
pp. 46-50
Author(s):  
Fatemeh Safari ◽  
Sheida Jodayri Zayer
Keyword(s):  
Cell Motility ◽  
Tumor Invasion ◽  
Cell Shape ◽  
Morphological Changes ◽  
Specific Inhibitor ◽  
Ags Cells ◽  
Transfected Cells ◽  
Family Protein ◽  
Epidermal Growth ◽  
Mammalian Protein

Introduction: Pragmin is the first mammalian protein that contains a functional the Glu-Pro-Ile-Tyr-Ala (EPIYA) motif. Pragmin was tyrosine phosphorylation by Src family kinases (SFKs), in response to epidermal growth factor (EGF) stimulation, and C-terminal Src kinase (CSK) at EPIYA motif. Pragmin transfected cells induced cell-morphological changes which were characterized by elongated cell shape with invasive phenotype that contributes to tumor invasion and metastasis. This study was established to investigate Src role as a key regulator of cell motility to induce elongated morphology of cells in Pragmin transfected cells by using PP2, a specific inhibitor of Src family protein kinase. Methods: Firstly, AGS cells were transfected by Pragmin and Pragmin mutant (Y391F) using lipofectamine 2000 reagent and then we treated the cells by PP2. Finally, we evaluated cell-morphological changes in the presence or the absence of PP2 by using light microscope and the results were analyzed. Results: Our results showed in AGS cells that were transiently transfected by Pragmin in the presence of PP2 (where Src activity was reduced), number of elongated cells were not changed compared to elongated cell numbers of Pragmin transfected cells in the absence of PP2. Conclusion: Our findings suggest that in spite of importance of Src to regulate the cell motility, cell-morphological changes of AGS transfected cells by Pragmin is independent on Src activity and it seems the other mechanism (s) are involved in these process.

Cell Motility in Tumor Invasion

2003 ◽  
Author(s):  
Alan Wells ◽  
Douglas A. Lauffenburger ◽  
Timothy Turner
Keyword(s):  
Cell Motility ◽  
Tumor Invasion

Cell Motility in Tumor Invasion

2004 ◽  
Author(s):  
Alan Wells ◽  
Douglas A. Lauffenburger ◽  
Timothy Turner
Keyword(s):  
Cell Motility ◽  
Tumor Invasion

Tumor invasion as dysregulated cell motility

2001 ◽  
Vol 11 (2) ◽  
pp. 105-117 ◽  
Author(s):  
Jareer Kassis ◽  
Douglas A Lauffenburger ◽  
Timothy Turner ◽  
Alan Wells
Keyword(s):  
Cell Motility ◽  
Tumor Invasion

scholarly journals FAK is required for the assembly of podosome rosettes

2011 ◽  
Vol 195 (1) ◽  
pp. 113-129 ◽  
Author(s):  
Yi-Ru Pan ◽  
Chien-Lin Chen ◽  
Hong-Chen Chen
Keyword(s):  
Extracellular Matrix ◽  
Cell Motility ◽  
Focal Adhesion Kinase ◽  
Intermediate Filaments ◽  
Focal Adhesion ◽  
Tumor Invasion ◽  
Matrix Degradation ◽  
Membrane Structures ◽  
Negative Role ◽  
Invasive Cell

Podosomes are dynamic actin-enriched membrane structures that play an important role in invasive cell motility and extracellular matrix degradation. They are often found to assemble into large rosettelike structures in highly invasive cells. However, the mechanism of this assembly remains obscure. In this study, we identified focal adhesion kinase (FAK) as a key molecule necessary for assembly. Moreover, phosphorylation of p130Cas and suppression of Rho signaling by FAK were found to be important for FAK to induce the assembly of podosome rosettes. Finally, we found that suppression of vimentin intermediate filaments by FAK facilitates the assembly of podosome rosettes. Collectively, our results strongly suggest a link between FAK, podosome rosettes, and tumor invasion and unveil a negative role for Rho signaling and vimentin filaments in podosome rosette assembly.

Linking altered cell motility and proteolytic activity to tumor invasion—An active role of CD97 in tumor progression

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 10103-10103
Author(s):  
G. Aust ◽  
M. Loeffler ◽  
I. Hanisch ◽  
M. Wobus ◽  
E. Wandel ◽  
...  
Keyword(s):  
Cell Motility ◽  
Tumor Cells ◽  
Proteolytic Activity ◽  
Tumor Invasion ◽  
Individual Cell ◽  
Active Role ◽  
Invasion Front

10103 Background: Tumor cells at the invasion front of several carcinomas differ in their molecule pattern from cells in central tumor regions. As recently shown by us, this includes the cell surface receptor CD97 (Am J Pathol 2002,161:1657–67). Here, we link related differences in cell biological and biomechanical properties to the characteristics of tumor invasion. We combine in vitro and in vivo experiments with computer simulations of tumor progression and analyze the particular role of CD97 in this process. Methods: We compared the cDNA pattern of clones with adjustable expression of normal or C- terminal truncated CD97 using microarrays and confirmed the results at the protein level. Clonal cell motility was analyzed by time-lapse video microscopy. The scid mouse model was used to monitor tumor growth in vivo. Additionally, we introduce a novel class of individual cell-based computer models of tumor invasion into stroma. The approach enables us to analyze the impact of different cellular alterations on the organization and dynamics of the tumor invasion front and we can study several assumptions about the origin of these alterations. Results: CD97 overexpression stimulates single cell motility and increases proteolytic activity and IL-8 secretion in vitro and promotes growth of tumors in scid mice. In contrast, tumor cells overexpressing truncated CD97 show lower proteolytic activity, impaired in vitro motility and in vivo tumor growth. By computer simulation studies we demonstrate that the observed effects induced by CD97 can strongly increase the invasion capacity of tumors. Furthermore, they can cause a specific morphology of the invasion front which is known to correlate with poor prognosis. Thus, as a consequence of our computer simulations and findings in vitro and in vivo, we suggest that CD97 plays an active role in the propagation of de-differentiated carcinomas. Conclusions: Our combined experimental and theoretical computer analysis provides a novel insight in how variations of individual cell properties can be linked to different patterns of tumor cell invasion. Our results suggest that proteolytic activity at the tumor front in conjunction with elevated and directed cell motility are key steps to aggressive tumor invasion. No significant financial relationships to disclose.

scholarly journals Growth Factor-Induced Cell Motility in Tumor Invasion

2002 ◽  
Vol 41 (2) ◽  
pp. 124-130 ◽  
Author(s):  
Alan Wells ◽  
Jareer Kassis ◽  
James Solava ◽  
Timothy Turner ◽  
Douglas A. Lauffenburger
Keyword(s):  
Growth Factor ◽  
Cell Motility ◽  
Tumor Invasion
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