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DcR1 expression in endometrial carcinomas
Jordi Tarragona1, Nuria Llecha, Maria Santacana
1Department of Pathology and Molecular Genetics, Hospital Universitari Arnau de Vilanova, University of Lleida IRBLLEIDA, Av Alcalde Rovira Roure 80, 25198 Lleida, Spain. tarragona@gss.scs.e
Abstract:
The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family, which mediates apoptosis by the extrinsic pathway. Up-regulation of decoy receptors, DcR1 and DcR2, may result in diminished binding of TRAIL to their functional receptors. DcR1 expression was assessed in normal endometrial tissue (NE) and endometrial carcinoma (EC) samples by immunohistochemistry (IHC) and quantitative real-time polymerase chain reaction (PCR). IHC was performed in two tissue microarrays; one composed of 80 samples of NE and a second one constructed from paraffin-embedded blocks of 62 EC. For quantitative real-time RT-PCR analysis, RNA was obtained from 19 NE and 28 EC samples using Trizol. mRNA expression of DcR1 was assessed with Taqman-based assays in an Abi-Prism 700 SDS. Results were correlated with stage, histological type, and grade. By IHC, cytoplasmic expression of DcR1 was frequently seen in NE (79.6%) and varied according to the menstrual cycle. Positive DcR1 immunostaining was also detected in EC (98.1% of the cases) without any specific statistical association with histological type, grade, and stage. By quantitative real-time PCR, all NE had similar levels of DcR1expression (0.8-1.7 RQ), which were considered the basal levels of DcR1 expression in NE. Increased DcR1 expression (> or =5-fold higher than the basal levels) was detected in 13 of 28 EC (46.4%). High DcR1 expression levels were found in ECs of different stages: IA, four of 12 (33%); IB, two of four (50%); IC, four of six (66%); and IIA and IIB three of six (50%). Results suggest that DcR1 expression occurs in a subset of EC and may contribute to resistance to TRAIL-induced apoptosis.
Insights
Decoy receptor 1 (DcR1) is frequently expressed in endometrial carcinoma (EC), potentially causing resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) therapy. This study assessed DcR1 expression in EC tissues.
Area of Science:
- Oncology
- Molecular Biology
- Cell Death Research
Background:
- The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) pathway is crucial for extrinsic apoptosis.
- Decoy receptors, such as DcR1, can inhibit TRAIL-mediated apoptosis by binding TRAIL, preventing it from activating functional death receptors.
- Understanding DcR1 expression in endometrial carcinoma (EC) is vital for developing targeted therapies.
Purpose of the Study:
- To investigate the expression levels of DcR1 in normal endometrial (NE) tissue and endometrial carcinoma (EC).
- To determine if DcR1 expression correlates with clinical parameters like stage, histological type, and grade in EC.
- To assess the potential role of DcR1 in TRAIL-induced apoptosis resistance in EC.
Main Methods:
- Immunohistochemistry (IHC) was used to assess DcR1 protein expression in tissue microarrays of 80 NE and 62 EC samples.
- Quantitative real-time PCR (RT-PCR) was employed to measure DcR1 mRNA expression in 19 NE and 28 EC samples.
- Results were statistically correlated with EC stage, histological type, and grade.
Main Results:
- Cytoplasmic DcR1 expression was observed in 79.6% of NE and 98.1% of EC samples by IHC.
- While DcR1 was frequently detected in EC, no significant association was found with histological type, grade, or stage.
- Quantitative RT-PCR revealed increased DcR1 mRNA expression (≥5-fold basal levels) in 46.4% of EC cases, with elevated levels across various stages.
Conclusions:
- DcR1 is commonly expressed in endometrial carcinoma.
- Increased DcR1 expression in a subset of EC may contribute to resistance to TRAIL-induced apoptosis.
- Targeting DcR1 could be a potential therapeutic strategy for overcoming TRAIL resistance in endometrial cancer.
