Abstract
Nonsteroidal anti-inflammatory drugs (NSAIDs) decrease the incidence of colon cancer. The underexpression of HLA antigens during colon cancer development is suspected to be a mechanism by which malignant cells escape immune surveillance. We examined whether NSAIDs affect the expression of HLA-DR in HT29 human colon adenocarcinoma cells, which do not express HLA-DR. Aspirin, indomethacin and sulindac induced several-fold the expression of HLA-DR in these cells in a concentration- and time-dependent manner. Aspirin increased HLA-DR alpha steady-state mRNA levels and HLA-DR alpha gene transcription rate. These findings raise the possibility that such a mechanism may be operative in vivo.
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