Altered growth regulation and enhanced tumorigenicity of NIH 3T3 fibroblasts transfected with protein kinase C-I cDNA.
Transfection of NIH 3T3 cells with plasmids containing rat brain protein kinase C-I (PKC-I) cDNA controlled by strong viral promoter/enhancer elements led to PKC-I gene expression as assessed by Northern analysis, cellular binding of phorbol ester, immunoblotting of cellular PKC, and membrane-associated PKC activity. While transfection did not induce foci, altered growth regulation was observed in established transfectant lines: transfectants displayed reduced dependence on serum for growth, grew to higher saturation densities, and displayed enhanced tumorigenicity when inoculated into nude mice. Continued high-level expression of PKC-I, however, may not be obligatory for the malignant phenotype in vivo. Tumors that retained transfected sequences had lower PKC-I transcript levels than the parental in vitro lines, suggesting an in vivo modulation. Our data show that PKC-I dysregulation leads to altered cell growth regulation and may be functionally equivalent to the action of tumor promoters.[1]References
- Altered growth regulation and enhanced tumorigenicity of NIH 3T3 fibroblasts transfected with protein kinase C-I cDNA. Persons, D.A., Wilkison, W.O., Bell, R.M., Finn, O.J. Cell (1988) [Pubmed]
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