Cited by 166Protein Kinase Regulation and GTPase SignalingCancer-related Molecular PathwaysT-cell and Retrovirus Studies

In vitro establishment is not a sufficient prerequisite for transformation by activated Ras oncogenes

Franza, B.Robert, Maruyama, Kazuo, Garrels, James I., Ruley, H.Earl·1986·Cell

Abstract

Activated ras genes transform REF52 cells only at low frequencies and adenovirus early region 1A collaborates with ras oncogenes to convert REF52 cells to a tumorigenic phenotype. While failure to transform did not result from an absence of ras gene expression, E1A appeared to enhance expression of transfected ras genes by approximately tenfold. However, enhanced ras expression alone does not account for collaboration by E1A since overexpression of T24 Ha-ras p21 induced morphological crisis and cell growth arrest rather than stable transformation. These results indicate that E1A contributes complementing biochemical activities that enable ras genes to transform REF52 and suggest that the role of E1A in primary cell transformation may extend beyond facilitating in vitro establishment.

Integrity signals

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Crossref · 10.1016/0092-8674(86)90462-9

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43 of 43 references verified0 citation errors · 0 not checkable

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  • REF52 cells are immortal fibroblasts but are similar to primary cells in that they display a high degree of growth control and require coexpression of a cooperating oncogene for transformation by ras.

    “REF52 cells are immortal fibroblasts but are similar to primary cells in that they display a high degree of growth control and require coexpression of a cooperating oncogene for transformation by ras (Franza et al. 1986).”

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Authors
Franza, B. R., Maruyama, K., Garrels, J. I., & Ruley, H. E.
Affiliations
  • Cold Spring Harbor Laboratory (US)
  • Massachusetts Institute of Technology (US)
Venue
Cell
Publisher
Elsevier BV
Published
1986-02
Volume
44
Issue
3
Pages
409-418
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2158195967
Cited by
166
References
43
Citations by year
2024: 4 · 2023: 3 · 2022: 1 · 2021: 2 · 2019: 1 · 2017: 1 · 2016: 3 · 2014: 2 · 2013: 3 · 2012: 2
FWCI
5.77
Type
journal article
Language
en
Open access
closed
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Cancer Society
  • National Cancer Institute
  • Cancer Research Institute
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and Retrovirus Studies
Keywords
oncogenic Ras, adenovirus E1A, cell transformation, growth arrest, tumorigenicity, oncogene cooperation, in vitro establishment
MeSH terms
Adenoviridae, Cell Line, Cell Transformation, Neoplastic, Enhancer Elements, Genetic, Genes, Viral, Neoplasm Proteins, Oncogenes, Transfection, Proto-Oncogene Proteins p21(ras)

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