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        <identifier>oai:figshare.com:article/34014609</identifier>
        <datestamp>2026-09-28T14:08:04Z</datestamp>
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          <dc:title>Data Sheet 1_Extracellular vesicle-mediated preconditioning of osteoblasts by ER+ breast cancer cells: implications for the bone metastatic niche.pdf</dc:title>
          <dc:creator>De Shanna M. Johnson (25122924)</dc:creator>
          <dc:creator>Edward A. Shangin (25122927)</dc:creator>
          <dc:creator>Hannah L. Marrone (25122930)</dc:creator>
          <dc:creator>Elisabeth J. Richardson (25122933)</dc:creator>
          <dc:creator>Danielle O. Barkers-Woode (25122936)</dc:creator>
          <dc:creator>Caitlyn J. Collins (13030521)</dc:creator>
          <dc:creator>L. Monet Roberts (25122939)</dc:creator>
          <dc:subject>Pharmacology</dc:subject>
          <dc:subject>breast-to-bone metastasis</dc:subject>
          <dc:subject>estrogen receptor positive (ER+)</dc:subject>
          <dc:subject>extracellular vesicles</dc:subject>
          <dc:subject>intercellular communication</dc:subject>
          <dc:subject>molecular mechanisms</dc:subject>
          <dc:description>&lt;p&gt;Breast cancer metastasis to bone most commonly occurs in late-stage disease and remains a major contributor to morbidity, reduced quality of life, and mortality, particularly in estrogen receptor-positive (ER+) tumors. Intercellular communication between tumor cells and bone-resident cells plays a critical role in promoting tumor invasion and development of metastatic bone lesions. Historically, tumor-bone interactions have been viewed largely through the lens of soluble factor-mediated signaling, particularly in the context of osteoclast-driven bone resorption and osteolytic lesion formation. However, the majority of bone metastases exhibit a mixed lytic and sclerotic phenotype, reflecting the combined involvement of osteoclast- and osteoblast-mediated remodeling. Here, we investigate how ER+ breast cancer-derived extracellular vesicle-enriched conditioned media influence osteoblast behavior and signaling in vitro, positioning osteoblasts as key intermediaries in bone metastatic progression. We first show that ER+ T47D cells release significantly higher EVs than MCF10A non-tumorigenic breast epithelial cells. Next, we demonstrate that osteoblasts actively internalize T47D-derived EVs by 24 h, resulting in significant alterations in their proliferation and signaling profiles associated with chemotaxis and vascular-associated pathways. Finally, we show that conditioned media from T47D EV-preconditioned osteoblasts did not significantly enhance breast tumor cell proliferation or overall motility outcomes. However, despite similar mean motility metrics between conditions, migration behavior exhibited distinct population-level distributions. Collectively, these findings demonstrate that ER+ breast cancer-derived EVs drive selective reprogramming of osteoblast signaling and function as an important component in tumor-bone niche conditioning.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-28T14:08:04Z</dc:date>
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          <dc:identifier>10.3389/fphar.2026.1844422.s001</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/Data_Sheet_1_Extracellular_vesicle-mediated_preconditioning_of_osteoblasts_by_ER_breast_cancer_cells_implications_for_the_bone_metastatic_niche_pdf/34014609</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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