Abstract
Downregulation of MHC Class I antigens has been observed in many cancers and usually results from a decreased gene transcription. A reporter CAT gene dependent on the MHC Class I κB site or on a longer promoter is transactivated by NF-κB complexes containing p65 or RelB. p100 as well as IκB-α are potent inhibitors of this transcription and p100 sequesters RelB and p65 complexes in the cytoplasm of breast cancer cells. However, although p100 is highly expressed in a number of breast cancer cell lines, MHC Class I antigen expression was observed on all the cell lines we analysed and could be further induced by stimulation with the cytokines IFN-γ or TNF-α. Stable transfection of a unresponsive mutated IκB-α Ser 32-36 expression vector showed that TNF-α induced MHC Cl I expression in an NF-κB-dependent way while IFN-γ did it independently of any NF-κB activation.
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Dejardin, E., Deregowski, V., Greimers, R. et al. Regulation of major histocompatibility complex class I expression by NF-κB-related proteins in breast cancer cells. Oncogene 16, 3299–3307 (1998). https://doi.org/10.1038/sj.onc.1201879
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DOI: https://doi.org/10.1038/sj.onc.1201879
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