{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T02:29:22Z","timestamp":1792981762763,"version":"4.5.0"},"reference-count":101,"publisher":"Oxford University Press (OUP)","license":[{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"am","delay-in-days":1,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"name":"American Society for Radiation Oncology (ASTRO)-Breast Cancer Research Foundation Career Development","id":[{"id":"https:\/\/ror.org\/02xjhr934","id-type":"ROR","asserted-by":"crossref"}]},{"name":"NCI-NIH","award":["R21CA249349"],"award-info":[{"award-number":["R21CA249349"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Triple-negative breast cancer requires new treatment strategies due to poor responses to current therapies. While myeloid SIRP\u03b1 mediates immunosuppression, its cancer intrinsic role remains poorly understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Human breast cancer scRNAseq profiles were used to examine SIRP\u03b1 expression across different cell populations and subtypes. TNBC brain-tropic cells were injected into the mouse mammary fat pad for the orthotopic tumor model and intracardiac-injected for brain metastasis models. Bulk RNA sequencing was used to determine SIRP\u03b1-regulated pathway. Stably SIRP\u03b1 overexpressed and knockout TNBC cell lines were established to determine SIRP\u03b1 intracellular regulation. Digital spatial profiling was utilized to investigate the orthotopic and brain metastasis tumor immune microenvironment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Human single-cell data showed that SIRP\u03b1 levels increased in malignant TNBC epithelial cells. We observed that SIRP\u03b1 is upregulated in patient breast-to-brain metastatic lesions. SIRP\u03b1 is overexpressed in TNBC brain-tropic cells compared to parental cells. Bulk RNA-Seq showed that targeting SIRP\u03b1 affects genes involved in mitochondrial dynamics, and that SIRP\u03b1 upregulates mitochondrial fission and induces metastasis through the SHP2\/Erk\/Drp1 signaling pathway. In vivo, overexpression of SIRP\u03b1 in cancer cells significantly increases TNBC systemic metastasis. Next, spatial proteomics revealed changes in the immune microenvironment associated with the SIRP\u03b1-regulated ECM protein fibronectin. Fibronectin induces microglial tolerance by impairing inflammatory signaling and metabolic reprogramming, allowing cancer to escape microglial immunosurveillance. Most importantly, SIRP\u03b1 inhibition reduced TNBC brain metastatic lesions in mouse metastasis models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Cancer-intrinsic SIRP\u03b1 promotes TNBC brain metastasis through increased mitochondria fission and triggering microglia tolerance, and targeting SIRP\u03b1 reduces brain metastasis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/neuonc\/noag202","type":"journal-article","created":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T04:19:51Z","timestamp":1788236391000},"source":"Crossref","is-referenced-by-count":1,"title":["Cancer-intrinsic SIRP\u03b1 signaling triggers mitochondrial fission and immune tolerance to promote triple-negative breast cancer breast-to-brain 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