Overexpression of protein kinase C-delta and -epsilon in NIH 3T3 cells induces opposite effects on growth, morphology, anchorage dependence, and tumorigenicity

J Biol Chem. 1993 Mar 25;268(9):6090-6.

Abstract

We have determined the patterns of mRNA and protein expression of 7 protein kinase C (PKC) isozymes in NIH 3T3 cells. Only PKC-alpha is expressed abundantly in NIH 3T3 cells; endogenous levels of the other 6 PKC isozymes are low or undetectable. We have overexpressed PKC-delta and -epsilon in these cells to observe activation/translocation of these two isozymes and the biological consequences of overexpression. Both PKC-delta and -epsilon, but not PKC-alpha, are partially associated with the insoluble fraction even in the absence of phorbol 12-myristate 13-acetate (PMA). Upon PMA stimulation, both PKC-delta and -epsilon translocate to the insoluble fraction of cell homogenates, as can be observed with the endogenous PKC-alpha. Overexpression of PKC-delta induces significant changes in morphology and causes the cells to grow more slowly and to a decreased cell density in confluent cultures. These changes are accentuated by treatment with PMA. Overexpression of PKC-epsilon does not lead to morphological changes, but causes increased growth rates and higher cell densities in monolayers. None of the PKC-delta overexpressers grow in soft agar with or without PMA, but all the cell lines that overexpress PKC-epsilon grow in soft agar in the absence of PMA, but not in its presence. NIH 3T3 cells that overexpress PKC-epsilon also form tumors in nude mice with 100% incidence. This indicates that high expression of PKC-epsilon contributes to neoplastic transformation.

MeSH terms

  • 3T3 Cells
  • Animals
  • Biological Transport
  • Blotting, Northern
  • Blotting, Western
  • Brain / enzymology
  • Cell Adhesion* / drug effects
  • Cell Division* / drug effects
  • Cell Transformation, Neoplastic*
  • Cloning, Molecular
  • Enzyme Activation
  • Enzyme Stability
  • Indoles / pharmacology
  • Isoenzymes / genetics
  • Isoenzymes / metabolism*
  • Kinetics
  • Maleimides / pharmacology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Nude
  • Neoplasms, Experimental / etiology
  • Protein Kinase C / genetics
  • Protein Kinase C / metabolism*
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • Indoles
  • Isoenzymes
  • Maleimides
  • Protein Kinase C
  • bisindolylmaleimide I
  • Tetradecanoylphorbol Acetate