Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1993-4-22
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
268
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6090-6
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:8454583-3T3 Cells, pubmed-meshheading:8454583-Animals, pubmed-meshheading:8454583-Biological Transport, pubmed-meshheading:8454583-Blotting, Northern, pubmed-meshheading:8454583-Blotting, Western, pubmed-meshheading:8454583-Brain, pubmed-meshheading:8454583-Cell Adhesion, pubmed-meshheading:8454583-Cell Division, pubmed-meshheading:8454583-Cell Transformation, Neoplastic, pubmed-meshheading:8454583-Cloning, Molecular, pubmed-meshheading:8454583-Enzyme Activation, pubmed-meshheading:8454583-Enzyme Stability, pubmed-meshheading:8454583-Indoles, pubmed-meshheading:8454583-Isoenzymes, pubmed-meshheading:8454583-Kinetics, pubmed-meshheading:8454583-Maleimides, pubmed-meshheading:8454583-Mice, pubmed-meshheading:8454583-Mice, Inbred C57BL, pubmed-meshheading:8454583-Mice, Nude, pubmed-meshheading:8454583-Neoplasms, Experimental, pubmed-meshheading:8454583-Protein Kinase C, pubmed-meshheading:8454583-Tetradecanoylphorbol Acetate
pubmed:year
1993
pubmed:articleTitle
Overexpression of protein kinase C-delta and -epsilon in NIH 3T3 cells induces opposite effects on growth, morphology, anchorage dependence, and tumorigenicity.
pubmed:affiliation
Laboratory of Genetics, National Cancer Institute, Bethesda, Maryland 20892.
pubmed:publicationType
Journal Article