Linked Life Data

8633212

Source:http://linkedlifedata.com/resource/pubmed/id/8633212

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pubmed-article:8633212pubmed:abstractTextA number of tumours and oncogene transformed cells displayed reduced MHC class I surface expression which seemed to enable their escape from immune surveillance. To test whether oncogenic activation is directly involved in suppressing MHC class I expression, a model of inducible oncogene expression was chosen. Mouse fibroblasts transfected with different oncogenes expressed under the control of the dexamethasone-inducible MMTV promoter were analysed in the presence and absence of hormone for the mRNA and protein expression of MHC class I molecules as well as the respective oncogenes. Immunofluorescence analyses demonstrated an inverse association of MHC class I and oncogene expression after dexamethasone stimulation, independent of the type of oncogene causing transformation. Hormone-mediated induction of oncogene expression caused down-regulation of all H-2 loci. Kinetic experiments using MMTV c-Ha-ras(A) transfectants revealed that down-regulation of MHC class I surface expression was preceded by a dexamethasone-induced change of morphology, anchorage-independent growth, and an increase of the ras protein p 21. Parallel monitoring of mRNA expression demonstrated a time-dependent up-regulation of ras specific transcripts, which was associated with differential regulation of MHC class I heavy and light chain transcripts. Beta2-microglobulin transcripts were transiently suppressed, whereas MHC class I heavy chain transcripts remained unaffected. To investigate the mechanisms of oncogene-mediated down-regulation of MHC class I expression, H-2 promoter transfections and a nuclear run on assays were performed. In MMTV c-Ha-ras(A) cells, neither alterations of the H-2 promoter activity nor of the transcriptional activity of H-2 antigens was observed in the presence of dexamethasone, whereas both could be up-regulated by interferon-gamma treatment. These data suggest that oncogene-mediated transformation is directly associated with MHC class I down-regulation, but that complex interactions affecting MHC class I heavy and light chain genes at the transcriptional and/or post-transcriptional level are involved in this process.lld:pubmed
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pubmed-article:8633212pubmed:volume43lld:pubmed
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pubmed-article:8633212pubmed:pagination537-44lld:pubmed
pubmed-article:8633212pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:8633212pubmed:year1996lld:pubmed
pubmed-article:8633212pubmed:articleTitleMultiple levels of MHC class I down-regulation by ras oncogenes.lld:pubmed
pubmed-article:8633212pubmed:affiliationJohannes Gutenberg-University, Third Department of Internal Medicine, Mainz, Germany.lld:pubmed
pubmed-article:8633212pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:8633212pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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