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SHR Neuro Krebs Kardio Lipid

Ritter, C; Fan, K; Paulson, KG; Nghiem, P; Schrama, D; Becker, JC.
Reversal of epigenetic silencing of MHC class I chain-related protein A and B improves immune recognition of Merkel cell carcinoma.
Sci Rep. 2016; 6:21678-21678 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG


Autor/innen der Med Uni Graz:
Becker Jürgen Christian
Fan Kaiji
Ritter Cathrin
Schrama David

Dimensions Citations:

Plum Analytics:
Number of Figures: 6
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Merkel cell carcinoma (MCC) is a virally associated cancer characterized by its aggressive behavior and strong immunogenicity. Both viral infection and malignant transformation induce expression of MHC class I chain-related protein (MIC) A and B, which signal stress to cells of the immune system via Natural Killer group 2D (NKG2D) resulting in elimination of target cells. However, despite transformation and the continued presence of virally-encoded proteins, MICs are only expressed in a minority of MCC tumors in situ and are completely absent on MCC cell lines in vitro. This lack of MIC expression was due to epigenetic silencing via MIC promoter hypo-acetylation; indeed, MIC expression was re-induced by pharmacological inhibition of histone deacetylases (HDACs) both in vitro and in vivo. This re-induction of MICs rendered MCC cells more sensitive to immune-mediated lysis. Thus, epigenetic silencing of MICs is an important immune escape mechanism of MCCs.
Find related publications in this database (using NLM MeSH Indexing)
Acetylation - drug effects
Animals -
Carcinoma, Merkel Cell - drug therapy
Carcinoma, Merkel Cell - genetics
Carcinoma, Merkel Cell - immunology
Carcinoma, Merkel Cell - pathology
Cell Line, Tumor -
Cytotoxicity, Immunologic -
Gene Silencing - drug effects
Gene Silencing - immunology
Histocompatibility Antigens Class I - genetics
Histocompatibility Antigens Class I - immunology
Histone Deacetylase Inhibitors - pharmacology
Histone Deacetylases - genetics
Histone Deacetylases - immunology
Histones - genetics
Histones - immunology
Humans -
Hydroxamic Acids - pharmacology
Killer Cells, Lymphokine-Activated - cytology
Killer Cells, Lymphokine-Activated - drug effects
Killer Cells, Lymphokine-Activated - immunology
Mice -
Mice, Inbred NOD -
NK Cell Lectin-Like Receptor Subfamily K - genetics
NK Cell Lectin-Like Receptor Subfamily K - immunology
Plicamycin - analogs & derivatives
Plicamycin - pharmacology
Promoter Regions, Genetic - drug effects
Signal Transduction -
Skin Neoplasms - drug therapy
Skin Neoplasms - genetics
Skin Neoplasms - immunology
Skin Neoplasms - pathology
Vorinostat -
Xenograft Model Antitumor Assays -

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