Changes in NF-kappa B and ISGF3 DNA binding activities are responsible for differences in MHC and beta-IFN gene expression in Ad5- versus Ad12-transformed cells
| Autor: | L E Babiss, S.G. Zimmer, U. Nielsch |
|---|---|
| Rok vydání: | 1991 |
| Předmět: |
Genes
Viral CD74 viruses Molecular Sequence Data CD1 Gene Expression Genes MHC Class I C-C chemokine receptor type 7 General Biochemistry Genetics and Molecular Biology MHC class I Animals RNA Messenger Molecular Biology Cell Line Transformed Binding Sites Base Sequence General Immunology and Microbiology biology Antigen processing Adenoviruses Human General Neuroscience NF-kappa B DNA Interferon-Stimulated Gene Factor 3 Interferon-beta Transporter associated with antigen processing biochemical phenomena metabolism and nutrition MHC restriction Cell Transformation Viral Rats Cell biology DNA-Binding Proteins Immunology biology.protein Adenoviruses Simian CD8 Research Article Transcription Factors |
| Zdroj: | The EMBO Journal. 10:4169-4175 |
| ISSN: | 0261-4189 |
| DOI: | 10.1002/j.1460-2075.1991.tb04995.x |
| Popis: | Changes in MHC class I expression are frequently observed in tumors, which represents at least one mechanism by which tumor cells escape immune surveillance. MHC class I expression is often suppressed in type 12 adenovirus (Ad12)-transformed rodent cells, but is highly induced in Ad5-transformed cells. This difference helps to explain why Ad12 but not Ad5 can induce tumors in immunocompetent syngeneic rats. In this report we demonstrate that only Ad5- but not Ad12-transformed rodent fibroblasts constitutively express beta-IFN which results in ISGF3 factor induction, and stimulation of MHC class I expression. Furthermore, we demonstrate that in contrast to Ad12-transformed cells, Ad5-transformed cells show constitutive levels of nuclear NF-kappa B-like DNA binding activity. This is of particular interest since both the beta-IFN and the MHC class I promoters contain an NF-kappa B DNA binding site. Thus, high levels of MHC class I expression in Ad5-transformed cells are due to a combinatorial stimulation of two cis-regulatory sequences of the MHC class I promoter: the NF-kappa B binding site and the interferon stimulated response element (ISRE), which binds the ISGF3 factor complex. The failure of Ad12-transformed cells to activate this pathway explains their low levels of MHC class I expression and their greater oncogenicity. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|