Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
9
|
| pubmed:dateCreated |
1992-12-21
|
| pubmed:abstractText |
In the presence of the glucocorticoid hormone dexamethasone, bovine papillomavirus-1 (BPV-1)-transformed C127 mouse fibroblasts assume a flattened morphology and reach a saturation density of only 50% of that attained without hormone. This phenotypic reversion of transformation is dependent on the continued presence of dexamethasone and occurs with concentrations as low as 1 nM. Dexamethasone also suppresses the growth of the parental C127 cells as well as that of cells transformed by polyoma middle-T. In contrast, the growth of C127 cells transformed by the oncogenes v-H-ras, v-mos, or v-fes is inhibited by low concentrations of dexamethasone (1 nM) and stimulated by higher concentrations (0.1-1 microM), possibly due to dexamethasone-induced transcription from the viral long terminal repeat promoters as is shown for v-H-ras. On the other hand, inhibition of BPV-transformed cell line growth by dexamethasone does not appear to be related to hormone effects on BPV-1 oncogene transcription. Indeed, in several cases, dexamethasone increases the steady state transcript levels of the BPV-1 oncogenes, E5 and E6-E7, while suppressing cellular proliferation. Dexamethasone also rapidly reduces the steady state levels of c-myc in the BPV-transformed cells but has less effect on c-myc expression in the ras-transformed cells. These results demonstrate that the growth-promoting actions of the papillomavirus transforming genes, but not those of several retroviral oncogenes, may be overcome by dexamethasone, which appears to act by down-regulation of c-myc expression.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Sep
|
| pubmed:issn |
0888-8809
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
6
|
| pubmed:geneSymbol |
c-myb,
c-myc,
ras,
v-Ha-ras,
v-fes,
v-mos
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1371-80
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:1331773-Animals,
pubmed-meshheading:1331773-Antigens, Polyomavirus Transforming,
pubmed-meshheading:1331773-Base Sequence,
pubmed-meshheading:1331773-Bovine papillomavirus 1,
pubmed-meshheading:1331773-Cell Division,
pubmed-meshheading:1331773-Cell Line, Transformed,
pubmed-meshheading:1331773-Cell Transformation, Viral,
pubmed-meshheading:1331773-Contact Inhibition,
pubmed-meshheading:1331773-Depression, Chemical,
pubmed-meshheading:1331773-Dexamethasone,
pubmed-meshheading:1331773-Fibroblasts,
pubmed-meshheading:1331773-Gene Expression Regulation, Viral,
pubmed-meshheading:1331773-Genes, Synthetic,
pubmed-meshheading:1331773-Mammary Neoplasms, Experimental,
pubmed-meshheading:1331773-Mice,
pubmed-meshheading:1331773-Molecular Sequence Data,
pubmed-meshheading:1331773-Oncogenes,
pubmed-meshheading:1331773-Polyomavirus,
pubmed-meshheading:1331773-Promoter Regions, Genetic,
pubmed-meshheading:1331773-Proto-Oncogene Proteins c-myc,
pubmed-meshheading:1331773-Retroviridae
|
| pubmed:year |
1992
|
| pubmed:articleTitle |
Glucocorticoid modulation of transformed cell proliferation is oncogene specific and correlates with effects on c-myc levels.
|
| pubmed:affiliation |
Department of Medicine, University of Rochester School of Medicine and Dentistry, New York 14642.
|
| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|