ArticleJournal of bone oncology2026
Recombinant LGR4 extracellular domain attenuates osteoclastogenesis and prevents bone metastasis via RANKL inhibition.
Article in Journal of bone oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
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Who cites it
1 citing paper in PubMed.
- Research Progress on Signaling Pathways in Breast Cancer Bone Metastasis.Oncology research · 2026Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Bone metastasis is a severe complication of advanced cancers, disrupting bone remodeling by hijacking the RANK/RANKL/OPG axis, which leads to excessive osteoclast activation and bone resorption. Current therapies, such as bisphosphonates and denosumab, offer limited survival benefits and carry significant safety risks, highlighting the need for novel agents that effectively inhibit osteolytic progression. Objective: This study aimed to evaluate the therapeutic potential of a recombinant extracellular domain of leucine-rich repeat-containing G-protein coupled receptor 4 (rLGR4-ECD), produced in CHO cells, to inhibit RANKL signaling, suppress osteoclastogenesis, and prevent bone metastasis in preclinical models. Methods: The human LGR4-ECD (residues 25-540) was cloned into the pcDNA4/TO vector and expressed in CHO-K1 cells. Stable monoclonal lines were established, and recombinant protein was purified via Ni-NTA affinity chromatography. Binding affinity to RANKL and RSPO4 was assessed by co-immunoprecipitation (co-IP). Results: rLGR4-ECD was successfully expressed and purified with over 95% purity and a yield of 2.38 mg/L. It bound specifically to RANKL and RSPO4 in co-IP assays. Conclusion: rLGR4-ECD effectively inhibits RANKL-induced osteoclastogenesis and reduces bone metastasis burden through specific suppression of osteoclast activity, leading to improved survival in a preclinical model. Its excellent efficacy and manufacturability support its potential as a novel therapeutic agent for bone metastatic disease.
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Registered trials
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