Analysis of the fibroblast transformation potential of GTPase-deficient gip2 oncogenes.

  • Gupta S
  • Gallego C
  • Lowndes J
 et al. 
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Abstract

Expression of GTPase-deficient Gi2 alpha subunit (alpha i2) mutant polypeptides and overexpression of the wild-type alpha i2 polypeptide in Rat 1a, Swiss 3T3, and NIH 3T3 fibroblasts altered normal growth regulation and induced a loss of contact inhibition. In Rat 1a cells (but not in NIH 3T3 or Swiss 3T3 cells), expression of the GTPase-deficient alpha i2 mutant polypeptides allowed colony formation in soft agar, which correlated with a loss in anchorage dependence and a decreased serum requirement. The altered growth regulatory properties of Rat 1a cells induced by expression of alpha i2 mutant polypeptides was not significantly inhibited by cotransfection with a dominant negative Ha-ras mutant polypeptide (Asn-17rasH), indicating that the activated Gi2 membrane signal transduction protein is uniquely capable of altering the regulation of Rat 1a cell growth by a predominantly c-ras-independent mechanism. The results show that GTPase-deficient alpha i2 mutant polypeptides have the properties of an oncogene that can induce the phenotypic characteristics of transformation in Rat 1a cells but that only a subset of these changes is observed with NIH 3T3 and Swiss 3T3 cells.

Author-supplied keywords

  • 3T3 Cells
  • Animals
  • Antibodies
  • Antibodies: immunology
  • Cell Division
  • Cell Line
  • Cell Transformation, Neoplastic
  • Cell Transformation, Neoplastic: genetics
  • Fibroblasts
  • Fibroblasts: pathology
  • GTP Phosphohydrolases
  • GTP Phosphohydrolases: genetics
  • GTP Phosphohydrolases: metabolism
  • GTP-Binding Proteins
  • GTP-Binding Proteins: genetics
  • GTP-Binding Proteins: metabolism
  • Gene Expression Regulation, Enzymologic
  • Mice
  • Mutation
  • Oncogenes
  • Rats
  • Transforming Growth Factor alpha
  • Transforming Growth Factor alpha: immunology

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Authors

  • S K Gupta

  • C Gallego

  • J M Lowndes

  • C M Pleiman

  • C Sable

  • B J Eisfelder

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