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Updated: Oct 11, 2026

Single Cell Multiplex Reverse Transcription Polymerase Chain Reaction After Patch-clamp
Published on: June 20, 2018
Isolation and molecular characterization of the 5'-upstream region of the human TRAIL gene
1Department of Surgery, University of Texas Medical Branch, Galveston, Texas 77555-0536, USA.
Abstract:
TRAIL, a novel member of the TNF family, acts through membrane receptors to induce apoptosis of activated T lymphocytes and may represent a mechanism for the "immune escape" of certain cancers. Various cytokines appear to increase expression of other TNF family members; however, the regulation of TRAIL has not been defined. The purpose of this study was to assess molecular mechanisms regulating TRAIL gene expression in human colon cancers. In this study, we have cloned the human TRAIL (hTRAIL) promoter ( approximately 1.6 kb) and identified a number of putative transcription factor binding sites such as NFAT, AP-1 and Sp1 sequences which are important for the expression of other TNF family members. Transient transfections of 5'-deletion promoter constructs into either Caco-2 or HT29 colon cancer cells identified TRAIL promoter regions critical for both basal and interferon-gamma (IFN-gamma)-mediated induction. Furthermore, induction of TRAIL mRNA levels was demonstrated in HT29 and Caco-2 cells with IFN-gamma treatment suggesting an important role for this cytokine in TRAIL expression.
Insights
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) gene expression in colon cancer is regulated by specific promoter regions. Interferon-gamma (IFN-gamma) significantly induces TRAIL mRNA levels, highlighting its role in cancer immune escape.
Area of Science:
- Immunology
- Molecular Biology
- Oncology
Background:
- Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a TNF family member inducing apoptosis in activated T lymphocytes.
- TRAIL may facilitate cancer immune escape, but its gene expression regulation is undefined.
- Understanding TRAIL regulation is crucial for cancer therapy development.
Purpose of the Study:
- To investigate the molecular mechanisms regulating TRAIL gene expression in human colon cancer.
- To identify key regulatory elements within the human TRAIL (hTRAIL) promoter.
- To assess the role of cytokines, specifically interferon-gamma (IFN-gamma), in TRAIL expression.
Main Methods:
- Cloning of the approximately 1.6 kb human TRAIL (hTRAIL) promoter region.
- Identification of putative transcription factor binding sites (NFAT, AP-1, Sp1).
- Transient transfections of 5'-deletion promoter constructs into Caco-2 and HT29 colon cancer cells.
- Analysis of TRAIL mRNA levels following IFN-gamma treatment.
Main Results:
- Key TRAIL promoter regions critical for basal and IFN-gamma-mediated induction were identified.
- Interferon-gamma (IFN-gamma) treatment induced TRAIL mRNA levels in HT29 and Caco-2 cells.
- Putative transcription factor binding sites important for TNF family member expression were found in the hTRAIL promoter.
Conclusions:
- Specific promoter regions and transcription factors regulate hTRAIL gene expression.
- IFN-gamma plays a significant role in inducing TRAIL expression in colon cancer cells.
- These findings provide insights into TRAIL's role in colon cancer and potential therapeutic strategies.
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