Disease relevance of Stc1

• STC has also been linked to cancer, pregnancy, lactation, angiogenesis, organogenesis, cerebral ischemia, and hypertonic stress [1].
• Neoplastic adipocytes in well-differentiated liposarcomas also stained for STC-1, while the frequency of STC-1-positive cells was lower in high-grade liposarcomas [2].
• Interestingly, STC1 and STC2 are expressed in many tumor cell lines, and the expression of STC2 is enhanced by estradiol in breast cancer cells [3].
• STC did not increase cAMP in ROS 17/2.8 or UMR-108 osteosarcoma cells, OK kidney cells, fetal rat limb bones, or neonatal mouse calvariae, and similarly failed to increase urinary cAMP in rats [4].
• After pertussis toxin treatment (200 ng/ml; 5 h), the peptone- and cephalexin-induced CCK secretion was significantly reduced, suggesting the involvement of pertussis toxin-sensitive heterotrimeric G protein(s) in the secretory activity of STC-1 cells [5].

Psychiatry related information on Stc1

• Locomotor effects suggest that STC-1 also has a role in maternal behavior [6].

High impact information on Stc1

• In fish, STC1 is a hormone that is secreted by the corpuscles of Stannius and is involved in calcium and phosphate homeostasis [7].
• The stanniocalcin 1 (STC1) gene is expressed in a wide variety of tissues, including the kidney, prostate, thyroid, bone, and ovary [7].
• The murine stanniocalcin 1 gene is not essential for growth and development [7].
• STC1 protein is considered to have roles in many physiological processes, including bone development, reproduction, wound healing, angiogenesis, and modulation of inflammatory response [7].
• The mouse enteroendocrine cell line STC-1 and C57BL/6 mice are used for in vitro and in vivo studies, respectively [8].

Chemical compound and disease context of Stc1

• Effects of dibutyryl cAMP on stanniocalcin and stanniocalcin-related protein mRNA expression in neuroblastoma cells [9].

Biological context of Stc1

• Since then, STC homologs have been identified in various genomes including human, mouse, rat, Xenopus and zebrafish [10].
• Upregulated expression of stanniocalcin-1 during adipogenesis [2].
• Untreated 3T3-L1 cells displayed negligible amounts of STC-1, whereas 3T3-L1 cells, treated with an adipogenic cocktail, upregulated the expression of STC-1 concomitantly with acquisition of the adipocytic phenotype [2].
• We have also shown that expression of STC-1 confers increased resistance to hypoxic and oxidative stress in neurons [2].
• The kinetics of STC-1 expression during adipogenesis was investigated in 3T3-LI cells, which can be induced to adipocyte differentiation [2].

Anatomical context of Stc1

• In this report we have characterized the STC receptor and the functional targeting of ligand and receptor to mitochondria [1].
• Given this, our findings suggest that STC-1, also in terminally differentiated adipocytes, may function as a "survival factor", which contributes to the maintenance of the integrity of mature adipose tissue [2].
• We have previously reported a high expression of STC-1 in postmitotically differentiated neurons and megakaryocytes [2].
• Our results indicate that STC-1 can affect calcium homeostasis, bone and muscle mass and structure, and angiogenesis through effects on osteoblasts, osteoclasts, myoblasts/myocytes, and endothelial cells [11].
• Consequently, STC may act as a signaling molecule between the thecal-interstitial cell compartment and the corpus luteum and oocyte, thereby regulating the activity of these structures in some way [12].

Associations of Stc1 with chemical compounds

• The glycoprotein hormone stanniocalcin (STC) has originally been described in the teleost kidney [10].
• Immunogold electron microscopy revealed that STC was preferentially concentrated in the mitochondria of all nephron segments targeted by STC [1].
• Taking a step further to dissect the possible regulatory pathways involved, with the aid of phorbol 12-myristate 13-acetate or ionomycin, additive effects on STC gene expression were observed [13].
• Identification of signal transduction pathways that modulate dibutyryl cyclic adenosine monophosphate activation of stanniocalcin gene expression in neuroblastoma cells [13].
• Calcitriol upregulates STC1 and downregulates STC2 expression in the kidney [3].

Physical interactions of Stc1

• Electromobility shift assays using STC-1 nuclear extracts demonstrated the specific binding of PDX-1 protein to a specific regulatory region in the GIP promoter [14].

Regulatory relationships of Stc1

• Insulin-like growth factor I receptors are expressed by the enteroendocrine cell line STC-1: relationship with proliferation and cholecystokinin expression [15].
• As STC-1 cells express TGR5 mRNA, we examined whether bile acids induce GLP-1 secretion through TGR5 [16].

Other interactions of Stc1

• Stanniocalcin gene expression during mouse urogenital development: a possible role in mesenchymal-epithelial signalling [17].
• In most mammalian tissues, the stanniocalcin-1 gene (STC-1) produces a 50-kDa polypeptide hormone known as STC50 [18].
• In the non-pregnant state, STC gene expression was confined to the uterine lumenal epithelium [19].
• In the MC3T3-E1 osteogenic cell model, STC1 protein and mRNA were detectable throughout proliferation and differentiation stages but levels were relatively higher late during nodule formation/mineralization phases [20].
• The specific localization of STC1 to chondrocytes and muscle cells suggests a role for this protein in chondrogenic and myogenic differentiation [21].

Analytical, diagnostic and therapeutic context of Stc1

• To determine the role of STC1 in mammals, we generated Stc1-null mice by gene targeting [7].
• In situ hybridization revealed strong, specific hybridization over the thecal-interstitial cells of the ovarian stroma, whereas immunohistochemical analysis indicated that STC was present not only in the stroma, but also in the corpora lutea and oocyte of the developing follicle [12].
• These changes in STC-1 mice could not be explained by deficits in blood vessel formation, as vascularity in organs and skeletal tissues was increased as was induction of vascularity in response to femoral artery ligation [11].
• In the present study, using immunocytochemistry, we showed that STC1 protein is localized in the developing bone and muscle of the mouse fetus [21].
• Molecular cloning and characterization of mouse stanniocalcin cDNA [22].

References