p53-dependent expression of the stress-induced protein (SIP)

The mouse stress-induced protein (SIP) mRNA is activated in the pancreas with acute pancreatitis and in several cell lines in response to various stress agents. The SIP gene is alternatively spliced, generating two proteins (SIP 18 and SIP 27). Both proteins, located mainly in the nucleus, promote c...

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Bibliographic Details
Published in:European journal of cell biology 2002-05, Vol.81 (5), p.294-301
Main Authors: Tomasini, Richard, Azizi Samir, Amina, Pebusque, Marie-Josèphe, Calvo, Ezequiel L., Totaro, Serena, Dagorn, Jean Charles, Dusetti, Nelson J., Iovanna, Juan L.
Format: Article
Language:English
Subjects:
alternative splicing - transformation
Amino Acid Sequence
Animals
Antineoplastic Agents - metabolism
Carrier Proteins - genetics
Carrier Proteins - metabolism
Cell Transformation, Neoplastic
Cells, Cultured
cellular stress
Cloning, Molecular
Doxorubicin - metabolism
Fibroblasts - cytology
Fibroblasts - physiology
Gene Expression Regulation, Neoplastic
Genes, Reporter
Heat-Shock Proteins - genetics
Heat-Shock Proteins - metabolism
Humans
Mice
Molecular Sequence Data
Mutation
p53
Promoter Regions, Genetic
ras Proteins - genetics
ras Proteins - metabolism
Sequence Alignment
SIP
Tissue Distribution
Transcription, Genetic
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
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Summary:The mouse stress-induced protein (SIP) mRNA is activated in the pancreas with acute pancreatitis and in several cell lines in response to various stress agents. The SIP gene is alternatively spliced, generating two proteins (SIP 18 and SIP 27). Both proteins, located mainly in the nucleus, promote cell death when overexpressed in vitro. We show that induction by stress agents of the expression of SIP 18 and SIP 27 mRNAs, observed in human- and mouse-derived cell lines, is absent from cells with deleted, mutated or inactive p53, suggesting that regulation of SIP gene expression is dependent on p53. That hypothesis is consistent with the presence of a functional p53-response element within the promoter region of the mouse SIP gene and confirmed by the induction of SIP mRNA expression in mouse embryo fibroblasts upon activation of a p53-dependent pathway by transfection with ras V12 or ras V12/E1A. In conclusion, SIP being a proapoptotic gene induced through p53 activation could be a stress-induced gene with antitumour properties.
ISSN:0171-9335
1618-1298
DOI:10.1078/0171-9335-00248