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The link between bone-derived factors osteocalcin, fibroblast growth factor 23, sclerostin, lipocalin 2 and tumor bone metastasis

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Summary: Sclerostin is an important regulator of bone homeostasis through inhibition of the Wnt-signaling pathway and is involved in the pathogenesis of various skeletal diseases. Ongoing research highlights the therapeutic implications of sclerostin in different pathological conditions. Antisclerostin antibodies have been approved for osteoporosis treatment, and studies are being conducted to evaluate their effectiveness in other skeletal disorders and cancer.

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Uncarboxylated osteocalcin promotes proliferation and metastasis of MDA-MB-231 cells through TGF-beta/SMAD3 signaling pathway

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Summary: The study revealed that GluOC promotes the proliferation and metastasis of MDA-MB-231 cells by upregulating the expression of MMP2, MMP13, VEGF, IL-8, and PTHrP genes, and inducing EMT. The promoting effect of GluOC was reversed in MDA-MB-231 cells treated with a specific inhibitor of SMAD3, suggesting a potential target for preventing TNBC bone metastasis.

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Hypophosphatemia and FGF23 tumor-induced osteomalacia in two cases of metastatic breast cancer

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Summary: Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome characterized by dysregulation of phosphate and vitamin D metabolism due to overproduction of fibroblast growth factor 23 (FGF23) by tumors. This leads to bone pain and fractures, and is commonly associated with mesenchymal tumors but can also be linked to malignant tumors. Delayed diagnosis of TIO can lead to worsened functional status and early morbidity and mortality.

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Summary: Bone serves as a supportive framework for the body and plays a crucial role in regulating calcium homeostasis and hematopoietic function. Recent research has highlighted the endocrine function of bone, with bone-derived factors impacting local and global metabolism, influencing energy balance and metabolic diseases such as osteoporosis, obesity, and diabetes mellitus. These findings may lead to new insights into the pathophysiology of metabolic diseases and inform strategies for diagnosis, treatment, and prevention.

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Summary: Patients with advanced prostate cancer often develop skeletal metastases that can lead to fractures, disability, and increased mortality. Interactions between tumor cells and osteoblasts are believed to play a major role in the osteotropism of prostate cancer. Prostate cancer-derived extracellular vesicles (EVs) are emerging as key players in reprogramming osteoblasts and supporting the formation of premetastatic niches, explaining the complexity of prostate cancer osteotropism.

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Osteocalcin promotes bone mineralization but is not a hormone

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Plasma FGF23 is not elevated in prostate cancer

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Klotho expression in long bones regulates FGF23 production during renal failure

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Bone Formation Is Coupled to Resorption Via Suppression of Sclerostin Expression by Osteoclasts

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Regulation of Sclerostin Expression in Multiple Myeloma by Dkk-1: A Potential Therapeutic Strategy for Myeloma Bone Disease

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SOST Inhibits Prostate Cancer Invasion

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Maternal and Offspring Pools of Osteocalcin Influence Brain Development and Functions

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Altered Bone Development and Turnover in Transgenic Mice Over-Expressing Lipocalin-2 in Bone

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Lipocalin-2 ameliorates granulocyte functionality

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Osteoblasts Are a Major Source of inflammatory Cytokines in the Tumor Microenvironment of Bone Metastatic Breast Cancer

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Disruption of the Lcn2 gene in mice suppresses primary mammary tumor formation but does not decrease lung metastasis

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Lipocalin 2 promotes breast cancer progression

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