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Cell Growth & Differentiation, Vol 9, Issue 3 209-221, Copyright © 1998 by American Association of Cancer Research


ARTICLES

Rac1 and extracellularly regulated kinase activation are sufficient for E1A-dependent cooperative transformation of primary epithelial cells, but progression can only be modulated by E1A or Rac1

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

Ras transformation of fibroblast cell lines requires activation of multiple distinct signal pathways that act synergistically. E1A-ras cotransformation of primary epithelial cells is enhanced by distinct mutations in the second exon of E1A, resulting in "hypertransformation" and metastasis. The molecular and cellular differences in the in vitro properties of such transformed cells are characterized here. Hypertransformed cells grew faster and to higher saturation densities; had smaller, more refractile cell morphologies with pronounced actin microspikes; and were less adhesive when compared with wild-type (WT) E1A+ras-expressing cells. No significant differences were observed in extracellularly regulated kinase activity levels between the hypertransformed and WT transformed cells. Activated raf and Rac1 together were sufficient for transformation of primary epithelial cells with E1A, whereas neither alone was competent to cooperate with E1A. In the presence of activated ras and WT E1A, activated Rac1 expression effected all of the hypertransformation properties. Dominant-negative Rac1 expression was suppressive of the hypertransformation phenotype, including cell morphology, actin cytoskeletal structures, decreased growth rates, and increased adhesion. Thus, hypertransformation is not the result of extracellularly regulated kinase differences but can be effected by perturbations in Rac1 signals, as well as E1A 12S COOH-terminal mutants.


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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.