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-DRα steady-state mRNA levels and HLA-DRα gene transcription rate. These findings raise the possibility that such a mechanism may be operative in vivo.
| Original language | English |
|---|---|
| Pages (from-to) | 1207-1211 |
| Number of pages | 5 |
| Journal | International Journal of Oncology |
| Volume | 8 |
| Issue number | 6 |
| State | Published - 1996 |
Keywords
- aspirin
- colon cancer
- gene regulation
- HLA
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