Abstract
Deficient expression of the mouse proto-oncogene PML is associated with tumor immune evasion, occurring through down-regulated expression of genes involved in antigen processing and presentation. We investigated whether the defective antigen presentation found in human lung cancer cells could be restored by the human homolog of PML. PML induced the expression of MHC class I heavy chain and beta2-microglobulin at the level of transcription, thereby restoring defective antigen presentation resolved in some, but not all, lung cancer cell lines. Furthermore, the capacity of PML to restore antigen presentation required its targeting into nuclear bodies. These findings might have important application in the development of antitumor immunotherapeutic strategies.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigen Presentation / immunology*
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Histocompatibility Antigens Class I / biosynthesis
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Histocompatibility Antigens Class I / genetics
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Histocompatibility Antigens Class I / immunology*
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Histocompatibility Antigens Class I / metabolism
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Humans
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Lung Neoplasms / immunology*
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Mice
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Neoplasm Proteins / immunology*
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Neoplasm Proteins / metabolism
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Nuclear Proteins*
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Promyelocytic Leukemia Protein
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Protein Structure, Tertiary
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Proto-Oncogene Mas
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Transcription Factors / immunology*
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Transcription Factors / metabolism
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Tumor Suppressor Proteins
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Up-Regulation
Substances
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Histocompatibility Antigens Class I
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MAS1 protein, human
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Neoplasm Proteins
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Nuclear Proteins
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Pml protein, mouse
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Promyelocytic Leukemia Protein
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Proto-Oncogene Mas
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Transcription Factors
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Tumor Suppressor Proteins
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PML protein, human