ArticleJournal for immunotherapy of cancer2025
RANKL blockade inhibits cancer growth through reversing the tolerogenic profile of tumor-infiltrating (plasmacytoid) dendritic cells.
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- A 'three-axis synergy' immunotherapeutic strategy for malignant bone tumors based on natural bioactives and bioactive materials.Bioactive materials · 2026Review
- Spatial organization of the TNBC tumor microenvironment: multicellular niches, T-cell bottlenecks, and therapeutic opportunities.Journal of translational medicine · 2026Review
- Breaking the immune "cold niche" in bone metastasis: core mechanisms of the multidimensional interwoven regulatory network and precision breakthrough strategies.Molecular cancer · 2026Review
- DC-intrinsic SHP1 restrains central memory CD8⁺ T cell formation via the TCF-1/Wnt/β-Catenin axis.Medical oncology (Northwood, London, England) · 2026Article
- Efficacy and safety of combined RANKL and PD-1 inhibitors in bone metastases: a retrospective study.Translational cancer research · 2026Article
- Hijacking the bone niche: mechanistic insights into bone metastasis in breast cancer.Bone research · 2026Review
- A conceptual blueprint for "turning cold to hot" in Osteosarcoma: from TME stratification hypotheses to adaptive therapeutic prospects.Cell communication and signaling : CCS · 2026Review
- Research Progress on Signaling Pathways in Breast Cancer Bone Metastasis.Oncology research · 2026Review
- CPT1A inhibition alleviates plasmacytoid dendritic cell-mediated immune suppression in colon cancer through fatty acid oxidation modulation.Journal for immunotherapy of cancer · 2025Article
- Advances in hydrogel-based materials for breast cancer bone metastasis: from targeted drug delivery to bone microenvironment remodeling.Frontiers in pharmacology · 2025Review
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18 authors.
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Abstract
backgroundOriginally identified for its involvement in bone remodeling, accumulating data emerged in the past years indicating that receptor activator of nuclear factor κB ligand (RANKL) actually acts as a multifunctional soluble molecule that influences various physiological and pathological processes. Regarding its role in carcinogenesis, while direct effects on tumor cell behavior have been precisely characterized, the impact of the RANKL/RANK system (and its inhibition) on the intratumoral immune landscape remains unclear.
methodsAfter various in silico/in situ/in vitro analyses, the immunotherapeutic efficacy of RANKL blockade (alone and in combination with immune checkpoint inhibitors (anti-programmed cell death protein-1 (PD-1)) or doxorubicin/paclitaxel-based chemotherapy) was investigated using different syngeneic mouse models of triple-negative breast cancer (4T1, 67NR and E0771). Isolated from retrieved tumors, 14 immune cell (sub)populations, along with the activation status of antigen-presenting cells, were thoroughly analyzed in each condition. Finally, the impact of RANKL on the functionality of both dendritic cells (DC) and plasmacytoid dendritic cells (pDC) was determined.
resultsA drastic tumor growth inhibition was reproductively observed following RANKL inhibition. Strikingly, this antitumor activity was not detected in immunocompromised mice, demonstrating its dependence on the adaptive immune responses and justifying the diverse enriched signatures linked to immune cell regulation/differentiation detected in RANKL
conclusionsTaken together, this study provides insight into the role of RANKL/RANK axis in immune tolerance, demonstrates the significant impact of RANKL-dependent impairment of T cell-DC/pDC crosstalk on tumor development and, ultimately, supports that this ligand could be an interesting actionable target for cancer immunotherapy.
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