CG&D
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fischer, R. S.
Right arrow Articles by Quinlan, M. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fischer, R. S.
Right arrow Articles by Quinlan, M. P.

Cell Growth & Differentiation, Vol 9, Issue 11 905-918, Copyright © 1998 by American Association of Cancer Research


ARTICLES

Identification of a novel mechanism of regulation of the adherens junction by E1A, Rac1, and cortical actin filaments that contributes to tumor progression

RS Fischer and MP Quinlan
Department of Microbiology & Immunology, University of Tennessee Health Science Center, Memphis 38163, USA.

Transformation progression toward more malignant behavior often results from a loss of epithelial cell behavior, especially cell-cell adhesion. E1A cooperates with ras to transform primary epithelial cells such that they maintain epithelial cell differentiation, including the proper localization of adherens junctions (AJs). Second exon mutants of E1A 12S cooperate with ras to produce a more aggressively transformed phenotype, termed hypertransformation, that includes the loss of adhesion. Such hypertransformation can also be achieved by the addition of activated Rac1 to cells expressing wild-type E1A and ras, suggesting that actin reorganization may be important for the hypertransformed phenotype. Primary epithelial cells expressing hypertransforming mutants of E1A or V12Rac1 exhibit the loss of cortical actin filaments. In these cells, AJ complexes do not incorporate alpha-catenin, fail to associate with the cytoskeleton, and fail to localize to the plasma membrane, resulting in the destabilization of the AJ components and a loss of function. Loss of these epithelial cell characteristics predisposes these cells to a more malignant phenotype due to the loss of cell-cell adhesion. Taken together, these results suggest a novel mechanism of regulation of AJ function in tumor progression that involves the correct targeting of the AJ components, and this is affected by the status of cortical actin, which can be differentially affected by E1A or Rac1.


This article has been cited by other articles:


Home page
J. Immunol.Home page
Y. M. Morillon, E. C. Lessey-Morillon, M. Clark, R. Zhang, B. Wang, K. Burridge, and R. Tisch
Antibody Binding to CD4 Induces Rac GTPase Activation and Alters T Cell Migration
J. Immunol., November 1, 2016; 197(9): 3504 - 3511.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
J. Jung, W. Cai, H. K. Lee, M. Pellegatta, Y. K. Shin, S. Y. Jang, D. J. Suh, L. Wrabetz, M. L. Feltri, and H. T. Park
Actin Polymerization Is Essential for Myelin Sheath Fragmentation during Wallerian Degeneration
J. Neurosci., February 9, 2011; 31(6): 2009 - 2015.
[Abstract] [Full Text] [PDF]


Home page
J. Cell Sci.Home page
M. Lindqvist, Z. Horn, V. Bryja, G. Schulte, P. Papachristou, R. Ajima, C. Dyberg, E. Arenas, T. P. Yamaguchi, H. Lagercrantz, et al.
Vang-like protein 2 and Rac1 interact to regulate adherens junctions
J. Cell Sci., February 1, 2010; 123(3): 472 - 483.
[Abstract] [Full Text] [PDF]


Home page
JCBHome page
H. Reuveni, T. Geiger, B. Geiger, and A. Levitzki
Reversal of the Ras-Induced Transformed Phenotype by Hr12, a Novel Ras Farnesylation Inhibitor, Is Mediated by the Mek/ERK Pathway
J. Cell Biol., December 11, 2000; 151(6): 1179 - 1192.
[Abstract] [Full Text] [PDF]


Home page
J. Cell Sci.Home page
F. G. Scholl, C. Gamallo, S. Vilar?o, and M. Quintanilla
Identification of PA2.26 antigen as a novel cell-surface mucin-type glycoprotein that induces plasma membrane extensions and increased motility in keratinocytes
J. Cell Sci., December 15, 1999; 112(24): 4601 - 4613.
[Abstract] [PDF]


Home page
Cell Growth Differ.Home page
M. P. Quinlan and J. L. Hyatt
Establishment of the Circumferential Actin Filament Network Is a Prerequisite for Localization of the Cadherin-Catenin Complex in Epithelial Cells
Cell Growth Differ., December 1, 1999; 10(12): 839 - 854.
[Abstract] [Full Text]


Home page
Cell Growth Differ.Home page
K. W. Foster, S. Ren, I. D. Louro, S. M. Lobo-Ruppert, P. McKie-Bell, W. Grizzle, M. R. Hayes, T. R. Broker, L. T. Chow, and J. M. Ruppert
Oncogene Expression Cloning by Retroviral Transduction of Adenovirus E1A-immortalized Rat Kidney RK3E Cells: Transformation of a Host with Epithelial Features by c-MYC and the Zinc Finger Protein GKLF
Cell Growth Differ., June 1, 1999; 10(6): 423 - 434.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1998 by the American Association of Cancer Research.