Linked Life Data

1698382

Source:http://linkedlifedata.com/resource/pubmed/id/1698382

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1990-11-5
pubmed:abstractText
In the present study, the effect of protease inhibitors on c-myc expression in normal and transformed C3H 10T1/2 cells was examined. Steady-state c-myc RNA levels were reduced in normal proliferating C3H 10T1/2 cells grown in medium containing antipain, leupeptin, and Bowman Birk inhibitor (BBI). These protease inhibitors have been shown previously to suppress transformation yields in carcinogen-exposed cells. A lesser reduction in c-myc RNA levels was observed when cells were grown in the presence of protease inhibitors that do not suppress carcinogenesis and when transformed C3H 10T1/2 cell populations were grown in the presence of the anticarcinogenic protease inhibitors. Studies to determine the effects of antipain on the stability of the c-myc message and on c-myc transcription rates were also performed. The half-life of the c-myc message increased from 10 to 40 min when cells were grown in antipain; cycloheximide further stabilized the c-myc message. Interestingly, nuclear run-off experiments showed that antipain had no effect on c-myc transcription rates. These data suggest that proteases may be involved in the regulation of c-myc RNA expression in normal C3H 10T1/2 cells, possibly by a posttranscriptional mechanism.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0899-1987
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
226-32
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Effects of protease inhibitors on c-myc expression in normal and transformed C3H 10T1/2 cell lines.
pubmed:affiliation
Department of Cancer Biology, Harvard School of Public Health, Boston, Massachusetts.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.