{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nStanniocalcin‐1 (STC1) is a multifunctional secreted glycoprotein originally discovered in bony fish that has evolved in mammals into a pleiotropic regulator of mineral homeostasis, cellular metabolism, and growth. In vivo studies show that transgenic overexpression of human STC1 in mice alters phosphate reabsorption, diminishes postnatal growth, and disrupts reproductive performance, while biochemical analyses have revealed that STC1 localizes predominantly to mitochondria—where it modulates electron transfer—and is expressed in mature adipocytes and growth plate chondrocytes, thereby influencing skeletal development and cell survival."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of cancer, STC1 expression is frequently up‐regulated under hypoxic conditions via HIF‑1–dependent mechanisms and further modulated by key transcriptional factors such as p53 and NF‑κB, promoting tumor cell survival, invasion, and metastasis. Elevated STC1 levels have been correlated with aggressive phenotypes across a broad range of malignancies—including ovarian, gastric, esophageal, colorectal, renal, and breast cancers—as well as gliomas and even acute leukemia—and contribute to autocrine and paracrine signaling loops that enhance angiogenesis (through interference with growth factor pathways such as VEGF and HGF), stimulate protease activity (for example by inhibiting pregnancy‐associated plasma protein‑A), and foster stem‐like traits that may underlie tumor dormancy and chemoresistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in tumor progression, STC1 serves as a critical modulator in vascular, inflammatory, and organ‐protective responses. Experimental models have shown that STC1 can attenuate inflammatory cell transmigration across endothelial barriers and promote neuroprotection following hypoxic preconditioning, while its actions in endothelial cells—mediated via interactions with VEGF and FGF‑2 signaling—contribute to angiogenic sprouting and stabilization of blood vessels. Moreover, STC1 has been demonstrated to reduce apoptosis and oxidative stress in models of optic neuropathy, diabetic kidney disease, and in the hematopoietic niche of acute myeloid leukemia, underscoring its potential as a therapeutic target to ameliorate tissue injury and aberrant remodeling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Robin Varghese, Anthony D Gagliardi, Peter E Bialek, et al. 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