Abstract |
Recent studies have suggested that certain oncogenes, in particular members of the myc family, may be involved in the down-regulation of HLA class-I antigen expression observed in many types of tumor. We report that constitutive expression of an OK10 v-myc gene in human monoblastic U-937 cells results in a reduced expression of HLA class-I cell-surface expression and decreased levels of HLA class-I protein and mRNA. All class-I alleles, with the possible exception of HLA A3, were affected, as shown by one-dimensional isoelectric focusing (ID-IEF). Basal expression of the beta 2m chain was also reduced, although to a lesser extent. In addition, we show that the PMA-, and at least partially the IFN-alpha-induced increase in HLA class-I antigen expression, was inhibited in U-937-myc cells both at the protein and the mRNA level. In contrast, the response to IFN-gamma was normal. Another important difference in the response to IFN-gamma and alpha was that, while IFN-gamma abrogated the v-myc block of PMA-induced differentiation of U-937 cells, as previously reported, IFN-alpha did not. Our data show that v-myc negatively affects the regulation of both basal and inducible HLA class-I antigen expression.
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Authors | L G Larsson, F Oberg, P Stöckbauer, M G Masucci, K Nilsson |
Journal | International journal of cancer
(Int J Cancer)
Vol. 52
Issue 5
Pg. 759-65
(Nov 11 1992)
ISSN: 0020-7136 [Print] United States |
PMID | 1358827
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antigens, CD
- CD11 Antigens
- Histocompatibility Antigens Class I
- Interferon-alpha
- RNA, Messenger
- Interferon-gamma
- Tetradecanoylphorbol Acetate
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Topics |
- Alleles
- Antigens, CD
(metabolism)
- CD11 Antigens
- Cell Division
- Cell Transformation, Viral
(genetics)
- Gene Expression Regulation
- Genes, myc
- Histocompatibility Antigens Class I
(genetics, metabolism)
- Humans
- Interferon-alpha
(pharmacology)
- Interferon-gamma
(pharmacology)
- Monocytes
(immunology, metabolism)
- RNA, Messenger
(genetics)
- Tetradecanoylphorbol Acetate
(pharmacology)
- Tumor Cells, Cultured
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