ArticleInternational journal of molecular sciences2018
TRAIL/NF-κB/CX3CL1 Mediated Onco-Immuno Crosstalk Leading to TRAIL Resistance of Pancreatic Cancer Cell Lines.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Exploring the causal relationship between CX3CL1 and prostate cancer prognosis using Mendelian randomization.Discover oncology · 2025Article
- Review
- Microglia govern the extinction of acute stress-induced anxiety-like behaviors in male mice.Nature communications · 2024Article
- Mechanisms underlying reversed TRAIL sensitivity in acquired bortezomib-resistant non-small cell lung cancer cells.Cancer drug resistance (Alhambra, Calif.) · 2024Article
- Article
- NF-κB and Pancreatic Cancer; Chapter and Verse.Cancers · 2021Review
- Clinical significance of expression level of CX3CL1-CX3CR1 axis in bone metastasis of lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021Article
- Research trends in pharmacological modulation of tumor-associated macrophages.Clinical and translational medicine · 2021Review
- Article
- Targets (Metabolic Mediators) of Therapeutic Importance in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2020Review
- Fractalkine/CX3CL1 in Neoplastic Processes.International journal of molecular sciences · 2020Review
- Regulation of pancreatic cancer TRAIL resistance by protein O-GlcNAcylation.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Stress Management: Death Receptor Signalling and Cross-Talks with the Unfolded Protein Response in Cancer.Cancers · 2020Review
- Stem Cells and Organoid Technology in Precision Medicine in Inflammation: Are We There Yet?Frontiers in immunology · 2020Review
- Macrophage and Tumor Cell Cross-Talk Is Fundamental for Lung Tumor Progression: We Need to Talk.Frontiers in oncology · 2020Review
- STK3 Suppresses Ovarian Cancer Progression by Activating NF-Journal of immunology research · 2020Article
- Article
- Review
- NF-κB Signaling in Targeting Tumor Cells by Oncolytic Viruses-Therapeutic Perspectives.Cancers · 2018Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignant neoplasms and registers rising death rates in western countries. Due to its late detection in advanced stages, its extremely aggressive nature and the minimal effectiveness of currently available therapies, PDAC is a challenging problem in the clinical field. One characteristic of PDAC is a distinct desmoplasia consisting of fibroblasts, endothelial and immune cells as well as non-cellular components, contributing to therapy resistance. It is well established that the NF-κB signaling pathway controls inflammation, cancer progression and apoptosis resistance in PDAC. This study attempts to identify NF-κB target genes mediating therapy resistance of humane PDAC cell lines towards death ligand induced apoptosis. By using a genome wide unbiased approach the chemokine CX3CL1 was established as a central NF-κB target gene mediating therapy resistance. While no direct impact of CX3CL1 expression on cancer cell apoptosis was identified in co-culture assays it became apparent that CX3CL1 is acting in a paracrine fashion, leading to an increased recruitment of inflammatory cells. These inflammatory cells in turn mediate apoptosis resistance of PDAC cells. Therefore, our data dissect a bifunctional cross-signaling pathway in PDAC between tumor and immune cells giving rise to therapy resistance.
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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.