ArticleJournal of orthopaedic surgery and research2023
GPR84 potently inhibits osteoclastogenesis and alleviates osteolysis in bone metastasis of colorectal cancer.
Article in Journal of orthopaedic surgery and research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Pharmacological modulation of GPR84 revealed by dual states structures and immune functional assays.Experimental & molecular medicine · 2026Article
- Fatty Acid-Sensing G Protein-Coupled Receptors in Skeletal Metabolism.Journal of bone metabolism · 2026Article
- The Role of G Protein-Coupled Receptors in the Regulation of Orthopaedic Diseases by Gut Microbiota.Nutrients · 2025Review
- Synthetic GPR84 Agonists in Colorectal Cancer: Effective in THP-1 Cells but Ineffective in BMDMs and MC38 Mouse Tumor Models.International journal of molecular sciences · 2025Article
- Organotropic metastasis in colorectal cancer: integrating molecular pathways with therapeutic opportunities.Frontiers in immunology · 2025Review
- Study on the knowledge, attitude and practice of single photon emission computed tomography among oncology healthcare professionals.Frontiers in public health · 2024Article
- Beyond boundaries: unraveling innovative approaches to combat bone-metastatic cancers.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The expression of GPR84 in bone marrow-derived monocytes/macrophages (BMMs) can inhibit osteoclast formation; however, its role in bone metastasis of colorectal cancer (CRC) is still unknown. To investigate the effects of GPR84 on bone metastasis of CRC, the murine CRC cell line MC-38 was injected into tibial bone marrow. We found that the expression of GPR84 in BMMs was gradually downregulated during bone metastasis of CRC, and the activation of GPR84 significantly prevented osteoclastogenesis in the tumor microenvironment. Mechanistically, the MAPK pathway mediated the effects of GPR84 on osteoclast formation. Moreover, we found that IL-11 at least partly inhibited the expression of GPR84 in the tumor microenvironment through the inactivation of STAT1. Additionally, activation of GPR84 could prevent osteolysis during bone metastasis of CRC. Our results suggest that CRC cells downregulate the expression of GPR84 in BMMs to promote osteoclastogenesis in an IL-11-dependent manner. Thus, GPR84 could be a potential therapeutic target to attenuate bone destruction induced by CRC metastasis.
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Registered trials
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