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Updated: Jun 2, 2026

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
Published on: July 22, 2020
Aspirin and aspirin-like drugs induce HLA-DR expression in HT29 colon cancer cells
P Arvind1, L Qiao, E Papavassiliou
1CORNELL UNIV,COLL MED,DEPT MED,NEW YORK,NY 10021.
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.
Insights
Nonsteroidal anti-inflammatory drugs (NSAIDs) increase HLA-DR expression in colon cancer cells, potentially enhancing immune surveillance. This suggests NSAIDs may impact colon cancer development by modulating immune responses.
Area of Science:
- Oncology
- Immunology
- Pharmacology
Background:
- Nonsteroidal anti-inflammatory drugs (NSAIDs) are known to reduce colon cancer incidence.
- Underexpression of Human Leukocyte Antigen (HLA) is implicated in colon cancer immune evasion.
- HT29 human colon adenocarcinoma cells lack baseline HLA-DR expression.
Purpose of the Study:
- To investigate the effect of NSAIDs on HLA-DR expression in colon adenocarcinoma cells.
- To determine if NSAIDs can restore HLA-DR expression in cells lacking it.
Main Methods:
- Treatment of HT29 cells with aspirin, indomethacin, and sulindac.
- Concentration- and time-dependent analysis of HLA-DR expression.
- Measurement of HLA-DR alpha steady-state mRNA levels and gene transcription rate.
Main Results:
- Aspirin, indomethacin, and sulindac significantly induced HLA-DR expression in HT29 cells.
- The induction of HLA-DR was concentration- and time-dependent.
- Aspirin treatment elevated HLA-DR alpha mRNA levels and gene transcription.
Conclusions:
- NSAIDs can upregulate HLA-DR expression in colon adenocarcinoma cells.
- This NSAID-mediated increase in HLA-DR may enhance immune surveillance against colon cancer.
- The findings suggest a potential in vivo mechanism for NSAIDs in colon cancer prevention.
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