ArticleInternational journal of molecular sciences2017
The Chemokine Receptor CXCR6 Evokes Reverse Signaling via the Transmembrane Chemokine CXCL16.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Cellular and inflammatory characteristics of patient‑derived glioblastoma organoids duringOncology reports · 2026Article
- The involvement of microglia and the CXCL16-CXCR6 axis in the recruitment of CD8Scientific reports · 2025Article
- Melanoma-Keratinocyte Crosstalk Participates in Melanoma Progression with Mechanisms Partially Overlapping with Those of Cancer-Associated Fibroblasts.International journal of molecular sciences · 2025Article
- Tumor-infiltrating nociceptor neurons promote immunosuppression.Science signaling · 2025Article
- A covalent creatine kinase inhibitor ablates glioblastoma migration and sensitizes tumors to oxidative stress.Scientific reports · 2024Article
- Pan-cancer mapping of single CD8Cell reports. Medicine · 2024Article
- A narrative review: CXC chemokines influence immune surveillance in obesity and obesity-related diseases: Type 2 diabetes and nonalcoholic fatty liver disease.Reviews in endocrine & metabolic disorders · 2023Review
- The Role of CXCL16 in the Pathogenesis of Cancer and Other Diseases.International journal of molecular sciences · 2021Review
- Cutaneous melanoma dissemination is dependent on the malignant cell properties and factors of intercellular crosstalk in the cancer microenvironment (Review).International journal of oncology · 2020Review
- Article
- Regulation of Chemokine-Receptor Interactions and Functions.International journal of molecular sciences · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reverse signaling is a signaling mechanism where transmembrane or membrane-bound ligands transduce signals and exert biological effects upon binding of their specific receptors, enabling a bidirectional signaling between ligand and receptor-expressing cells. In this study, we address the question of whether the transmembrane chemokine (C-X-C motif) ligand 16, CXCL16 is able to transduce reverse signaling and investigate the biological consequences. For this, we used human glioblastoma cell lines and a melanoma cell line as in vitro models to show that stimulation with recombinant C-X-C chemokine receptor 6 (CXCR6) or CXCR6-containing membrane preparations induces intracellular (reverse) signaling. Specificity was verified by RNAi experiments and by transfection with expression vectors for the intact CXCL16 and an intracellularly-truncated form of CXCL16. We showed that reverse signaling via CXCL16 promotes migration in CXCL16-expressing melanoma and glioblastoma cells, but does not affect proliferation or protection from chemically-induced apoptosis. Additionally, fast migrating cells isolated from freshly surgically-resected gliomas show a differential expression pattern for CXCL16 in comparison to slowly-migrating cells, enabling a possible functional role of the reverse signaling of the CXCL16/CXCR6 pair in human brain tumor progression in vivo.
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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.