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Integration of interferon-alpha/beta signalling to p53 responses in tumour suppression and antiviral defence
- Source :
- Nature. 424(6948)
- Publication Year :
- 2003
-
Abstract
- Swift elimination of undesirable cells is an important feature in tumour suppression and immunity. The tumour suppressor p53 and interferon-alpha and -beta (IFN-alpha/beta) are essential for the induction of apoptosis in cancerous cells and in antiviral immune responses, respectively, but little is known about their interrelationship. Here we show that transcription of the p53 gene is induced by IFN-alpha/beta, accompanied by an increase in p53 protein level. IFN-alpha/beta signalling itself does not activate p53; rather, it contributes to boosting p53 responses to stress signals. We show examples in which p53 gene induction by IFN-alpha/beta contributes to tumour suppression. Furthermore, we show that p53 is activated in virally infected cells to evoke an apoptotic response and that p53 is critical for antiviral defence of the host. Our study reveals a hitherto unrecognized link between p53 and IFN-alpha/beta in tumour suppression and antiviral immunity, which may have therapeutic implications.
- Subjects :
- Transcriptional Activation
Cell signaling
Tumor suppressor gene
Transcription, Genetic
medicine.medical_treatment
Alpha interferon
Apoptosis
Biology
Response Elements
Vesicular stomatitis Indiana virus
Mice
Immune system
Neoplasms
medicine
Tumor Cells, Cultured
Animals
Humans
RNA, Messenger
Interferon alfa
Regulation of gene expression
Multidisciplinary
Interferon-alpha
Interferon-Stimulated Gene Factor 3
Interferon-beta
Interferon-Stimulated Gene Factor 3, gamma Subunit
DNA-Binding Proteins
Gene Expression Regulation, Neoplastic
Mice, Inbred C57BL
Cytokine
Cell Transformation, Neoplastic
Immunology
Cancer research
Signal transduction
Tumor Suppressor Protein p53
medicine.drug
Signal Transduction
Transcription Factors
Subjects
Details
- ISSN :
- 14764687
- Volume :
- 424
- Issue :
- 6948
- Database :
- OpenAIRE
- Journal :
- Nature
- Accession number :
- edsair.doi.dedup.....62a9bea46edf4b0cc020344ebd3db77b