Linked Life Data

2174893

Source:http://linkedlifedata.com/resource/pubmed/id/2174893

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
35
pubmed:dateCreated
1991-1-23
pubmed:abstractText
Previous studies have demonstrated that expression of the c-jun proto-oncogene is induced by phorbol esters and other agents that activate protein kinase C. The present work has examined the involvement of cAMP-dependent signaling mechanisms in the regulation of c-jun gene expression. Low levels of c-jun transcripts were detectable in untreated HL-60 myeloid leukemia cells. In contrast, treatment of these cells with 8-bromoadenosine 3',5'-cyclic monophosphate was associated with increases in c-jun expression that were maximal at 3 h and then declined to pretreatment levels. Similar findings were obtained with N6,2'-O-dibutyryladenosine 3',5'-cyclic monophosphate and 8-(4-chlorophenylthio)-adenosine 3',5'-cyclic monophosphate, but not with 8-bromoguanosine 3',5'-cyclic monophosphate. c-jun transcripts were also increased with agents, such as prostaglandin E2 and forskolin, that increase intracellular cAMP levels. The effects of these agents on c-jun expression were associated with activation of cAMP-dependent protein kinase. Moreover, inhibition of this kinase activity with the isoquinolinesulfonamide derivative H8 was associated with a block in the induction of c-jun expression by cAMP. Nuclear run-on analysis further demonstrated that while c-jun transcription is a low levels in untreated HL-60 cells, treatment with cAMP analogs is associated with an increase in the transcriptional rate of this gene. Taken together, these findings suggested that, in addition to activation of protein kinase C, stimulation of cAMP-dependent protein kinase activity is also involved in the transcriptional induction of c-jun gene expression. The present results similarly demonstrate that c-fos gene transcription is induced in HL-60 cells through a mechanism involving cAMP-dependent protein kinase activity. Since heterodimers of the Jun and Fos proteins have been shown to bind to the phorbol ester-responsive element (AP-1-binding site), the present findings indicate that cAMP-induced signaling events may also regulate gene transcription through formation of Fos/Jun heterodimers and that interaction between phorbol ester- and cAMP-dependent pathways could occur through induction of the c-jun gene in these cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
265
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
22011-5
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Regulation of c-jun gene expression by cAMP in HL-60 myeloid leukemia cells.
pubmed:affiliation
Laboratory of Clinical Pharmacology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't