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Suppression of basal, PMA- and IFN-alpha-, but not IFN-gamma-induced expression of HLA class I in v-myc-transformed U-937 monoblasts.

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.
AuthorsL G Larsson, F Oberg, P Stöckbauer, M G Masucci, K Nilsson
JournalInternational journal of cancer (Int J Cancer) Vol. 52 Issue 5 Pg. 759-65 (Nov 11 1992) ISSN: 0020-7136 [Print] United States
PMID1358827 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antigens, CD
  • CD11 Antigens
  • Histocompatibility Antigens Class I
  • Interferon-alpha
  • RNA, Messenger
  • Interferon-gamma
  • Tetradecanoylphorbol Acetate
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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