ArticleAmerican journal of cancer research2019
DcR3 promotes proliferation and invasion of pancreatic cancer via a DcR3/STAT1/IRF1 feedback loop.
Article in American journal of cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed.
- DcR3, stabilized by the RNA-binding protein IGF2BP2, promotes proliferation, invasion, and migration of trophoblast cells and facilitates angiogenesis.BMC pregnancy and childbirth · 2025Article
- Gene Expression Profiling of Pancreatic Ductal Adenocarcinoma Arising From Intraductal Papillary Mucinous Neoplasms of the Pancreas.Cancer medicine · 2024Article
- Article
- Targeting caspase-8: a new strategy for combating hepatocellular carcinoma.Frontiers in immunology · 2024Review
- Research Progress of DcR3 in the Diagnosis and Treatment of Sepsis.International journal of molecular sciences · 2023Review
- Molecular profiling and specific targeting of gemcitabine-resistant subclones in heterogeneous pancreatic cancer cell populations.Frontiers in oncology · 2023Article
- A stable, engineered TL1A ligand co-stimulates T cells via specific binding to DR3.Scientific reports · 2022Article
- The Role of Feedback Loops in Targeted Therapy for Pancreatic Cancer.Frontiers in oncology · 2022Review
- Integrative analysis of TNFRSF6B as a potential therapeutic target for pancreatic cancer.Journal of gastrointestinal oncology · 2021Article
- Case-Control Study onPharmacogenomics and personalized medicine · 2020Article
- The Role of Decoy Receptor DcR3 in Gastrointestinal Malignancy.Cancer diagnosis & prognosisReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer (PC) is one of the most common gastrointestinal malignancies that are highly aggressive with a low 5-year survival rate. Accumulated evidence has indicated that decoy receptor 3 (DcR3) is involved in several pathologic processes and various cancers. However, the mechanisms underlying dysregulated DcR3 expression and activation in PC remain to be fully established. In this study, we investigate the function and regulatory network of DcR3 in PC. We found that DcR3 was upregulated in PC tissues and serum. High DcR3 expression was associated with aggressive clinicopathological features and poor prognosis. Functionally, DcR3 not only increased cell migration and invasion in vitro but also promoted tumour growth both in vitro and in vivo by loss-of-function and gain-of-function experiments. Mechanistically, DcR3 promoted the phosphorylation of signal transducers and activators of transcription 1 (STAT1), leading to a dramatic increase in interferon regulatory factor 1 (IRF1). IRF1 then increased the transcriptional activity of DcR3, forming a positive feedback loop to reinforce DcR3 expression. In addition, DcR3 promoted carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) expression through activated IRF1. In conclusion, our findings provided novel insights into the function and mechanism of DcR3 in the pathogenesis of PC, which may be a potential therapeutic target for PC.
Indexed as
Identifiers
31911850PMC6943350What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.