{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T02:17:11Z","timestamp":1792808231486,"version":"4.5.0"},"posted":{"date-parts":[[2026,8,10]]},"group-title":"Cancer Biology","reference-count":64,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,8,10]],"date-time":"2026-08-10T00:00:00Z","timestamp":1786320000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Prostate Cancer Research and Breast Cancer Now bone metastasis collaboration fund","award":["BMCF01"],"award-info":[{"award-number":["BMCF01"]}]},{"name":"Prostate Cancer UK","award":["RIA21-ST2-006"],"award-info":[{"award-number":["RIA21-ST2-006"]}]},{"name":"Medical Research Council","award":["MR\/R015902\/1"],"award-info":[{"award-number":["MR\/R015902\/1"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,8,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  Prostate cancer is a leading cause of cancer-related mortality in men, and effective treatment options are limited for advanced and metastatic disease. The sialoglycan immune checkpoint Siglec-15 has emerged as a key mediator of tumour-associated immune suppression in several malignancies; however, its expression and functional role in prostate cancer remain poorly defined. Here, using dual immunofluorescence and immunohistochemistry, we demonstrate that Siglec-15 is expressed by prostate tumour epithelial cells, immunosuppressive macrophage phenotypes, and bone-resorbing osteoclasts within the tumour microenvironment. Mechanistically, we show that direct Siglec-15 receptor crosslinking, either by antibodies or tumour cell-derived conditioned medium, promotes monocyte-to-macrophage differentiation, generating macrophages with immunosuppressive and pathogenic phenotypes. Using therapeutic antibodies, we show that Siglec-15 blockade suppresses supernatant-induced monocyte to macrophage differentiation, allowing for the recovery of CD8\u207a T-cell activation. Furthermore, we reveal that macrophage colony-stimulating factor (M-CSF) driven monocyte-derived macrophage differentiation is partially dependent on Siglec-15 signalling, with Siglec-15 blockade enhancing CD8\u207a T-cell responses. In addition, anti-Siglec-15 treatment suppressed osteoclast differentiation, highlighting a dual role for Siglec-15 in prostate cancer immune suppression and bone remodelling. Consistent with these\n                  <jats:italic>in vitro<\/jats:italic>\n                  findings, therapeutic Siglec-15 blockade significantly reduced subcutaneous tumour growth in a CD8\u207a T-cell-dependent manner and prolonged survival in a mouse model of prostate cancer metastasis. Together, these findings identify Siglec-15 as a central regulator of the prostate cancer glyco-immune axis, linking tumour-associated macrophage immune suppression with osteoclast-mediated bone remodelling, providing a compelling rationale for the clinical development of Siglec-15-targeted therapies for patients with advanced disease.\n                <\/jats:p>","DOI":"10.64898\/2026.08.07.743480","type":"posted-content","created":{"date-parts":[[2026,8,10]],"date-time":"2026-08-10T08:45:14Z","timestamp":1786351514000},"source":"Crossref","is-referenced-by-count":2,"title":["Siglec-15 is a glyco-immune checkpoint in prostate cancer regulating immune evasion and metastasis"],"prefix":"10.64898","author":[{"given":"Nicoll","family":"Matthews","sequence":"first","affiliation":[{"name":"Newcastle University Centre for Cancer, Newcastle University Institute of Biosciences, Newcastle, NE1 3BZ, 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