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these results suggest that mesenchymal stem cells protect vascular cells from inflammatory injury partially by secreting STC1
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Data indicate that stanniocalcin 1 (STC1) is a non-canonical NOTCH1 ligand and acts as a crucial regulator of stemness in glioblastoma (GBM).
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these data demonstrated that STC1 can promote cell apoptosis via NF-kappaB phospho-P65 (Ser536) by PI3K/AKT, IkappaBalpha and IKK signaling in cervical cancer cells
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Our results demonstrated the contrasting effects of STC1 and STC2-derived peptides on human macrophage foam cell formation associated with ACAT1 expression and on HASMC migration.
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Ssecretory STC1 enhances metastatic potential of hepatocellular carcinomas via JNK signaling.
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Glycolysis from glucose is regulated by hSTC-1, decreasing the adequate supply of glycerol-3-phosphate (G3P) needed for fatty acid esterification and triacylglycerol (TG) storage in brown adipose tissue (BAT). The decrease of TG capacity synthesis from glucose by hSTC-1 compromises the BAT thermogenic capacity.
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Increased STC1 plasma level represents a hallmark of late-onset preeclampsia; STC1 gene variants modulate placental gene expression and maternal hormone levels.
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Latanoprost-induced reduction of intraocular pressure is mediated through the downstream signaling molecule STC-1. When used by itself, STC-1 exhibits ocular hypotensive properties.
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Study demonstrates that STC1 is overexpressed in the prostate carcinoma cell lines and suggests that it promotes prostate carcinoma cell proliferation via cyclin E1/CDK2.
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In the fed state, STC1 increases the incorporation of (14)C from glucose into lipids in the white retroperitoneal adipose tissue (WRAT). STC1 is one of the hormonal factors that control glucose metabolism in WRAT in the fed state.
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STC1 protein is significantly up-regulated in midsecretory endometrial fluid and is dysregulated in eutopic endometrial tissue from women with endometriosis. It is likely regulated by cAMP and may be involved in the pathogenesis of decidualization defects.
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STC1 expression is significantly upregulated in human masticatory mucosa during wound healing
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elevated STC-1 expression is associated with poor clinical outcome in triple-negative breast cancer (TNBC) patients, and STC-1 is directly involved in the invasiveness of TNBC cells
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we demonstrated that aberrant STC1 expression is associated with poor prognosis and stimulates the invasiveness of triplenegative breast cancer cells
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our findings strongly suggest that elevated expression of STC1 protein at the III-IV stage of lung adenocarcinoma promotes tumorigenesis of lung adenocarcinoma and positively associates with the cancer progression, which may be of potential value as tumor marker in clinical tracking lung adenocarcinoma progression.
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Data suggest that stanniocalcin 1 and 2 (STC1, STC2) participate in inhibition of proteolytic activity of pregnancy-associated plasma protein-A (PAPP-A) during folliculogenesis.
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STC1 gene expression at diagnosis might be a useful prognostic marker for clinical outcome and monitoring therapeutic response in patients with acute leukemia.
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STC1 blunts bleomycin-induced rise in thrombin protein and activity, diminishes thrombin-induced signaling through PAR1 to ERK, and inhibits bleomycin-induced pneumonitis.
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Data revealed the existence of a moderating effect between Klotho and STC1, where Klotho may inhibit thyroid tumor progression by inhibiting the tumor marker level of STC1.
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High expression levels of stanniocalcin-1 is associated with Hepatocellular Carcinoma.
