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We identified a membrane\u2013bound splice variant, ER\u03b136, in TNBC cells that responds to estrogen (E2) and may contribute to bone osteolysis. We demonstrated that the MDA-MB-231 TNBC cell line, which expresses ER\u03b136 similarly to MCF7 cells, is responsive to E2, forming osteolytic tumors in vivo. MDA-MB-231 cells activate osteoclasts in a paracrine manner. Conditioned media (CM) from MDA-MB-231 cells treated with bovine serum albumin\u2013bound E2 (E2-BSA) increased activation of human osteoclast precursor cells; this was blocked by addition of anti\u2013ER\u03b136 antibody to the MDA-MB-231 cultures. Osteoclast activation and bone resorption genes were elevated in RAW 264.7 murine macrophages following treatment with E2-BSA\u2013stimulated MDA-MB-231 CM. E2 and E2-BSA increased phospholipase C (PLC) and protein kinase C (PKC) activity in MDA-MB-231 cells. To examine the role of ER\u03b136 signaling in bone osteolysis in TNBC, we used our bone\u2013cancer interface mouse model in female athymic homozygous Foxn1nu mice. Mice with MDA-MB-231 tumors and treated with tamoxifen (TAM), E2, or TAM\/E2 exhibited increased osteolysis, cortical bone breakdown, pathologic fracture, and tumor volume; the combined E2\/TAM group also had reduced bone volume. These results suggest that E2 increased osteolytic lesions in TNBC through a membrane\u2013mediated PLC\/PKC pathway involving ER\u03b136, which was enhanced by TAM, demonstrating the role of ER\u03b136 and its membrane\u2013associated signaling pathway in bone tumors. This work suggests that ER\u03b136 may be a potential therapeutic target in patients with TNBC.<\/jats:p>","DOI":"10.1093\/jbmrpl\/ziae041","type":"journal-article","created":{"date-parts":[[2024,3,27]],"date-time":"2024-03-27T03:06:02Z","timestamp":1711508762000},"source":"Crossref","is-referenced-by-count":5,"title":["Estradiol induces bone osteolysis in triple\u2013negative breast cancer via its membrane\u2013associated receptor ER\u03b136"],"prefix":"10.1093","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1212-6164","authenticated-orcid":false,"given":"D Joshua","family":"Cohen","sequence":"first","affiliation":[{"name":"Department of Biomedical Engineering, Virginia Commonwealth University , Richmond, VA 23284 , United States"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cydney D","family":"Dennis","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, Virginia Commonwealth University , Richmond, VA 23284 , United States"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jingyao","family":"Deng","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, Virginia Commonwealth University , Richmond, VA 23284 , United States"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Barbara D","family":"Boyan","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, Virginia Commonwealth University , Richmond, VA 23284 , United States"},{"name":"Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology , Atlanta, GA 30332 , United States"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zvi","family":"Schwartz","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, Virginia Commonwealth University , Richmond, VA 23284 , United States"},{"name":"Department of Periodontics, The University of Texas Health Science Center at San Antonio , San Antonio, TX 78229 United States"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2024,3,26]]},"reference":[{"issue":"1","key":"2024042100254953800_ref1","doi-asserted-by":"crossref","first-page":"7","DOI":"10.3322\/caac.21708","article-title":"Cancer statistics, 2022","volume":"72","author":"Siegel","year":"2022","journal-title":"CA Cancer J 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