PHOENIX SECRETOMICS . Human Decorin 359 amino acid, MW 39747Da |
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MKATIILLLL AQVSWAGPFQ QRGLFDFMLE DEASGIGPEV PDDRDFEPSL GPVCPFRCQC HLRVVQCSDL GLDKVPKDLP PDTTLLDLQN NKITEIKDGD FKNLKNLHAL ILVNNKISKV SPGAFTPLVK LERLYLSKNQ LKELPEKMPK TLQELRAHEN EITKVRKVTF NGLNQMIVIE LGTNPLKSSG IENGAFQGMK KLSYIRIADT NITSIPQGLP PSLTELHLDG NKISRVDAAS LKGLNNLAKL GLSFNSISAV DNGSLANTPH LRELHLDNNK LTRVPGGLAE HKYIQVVYLH NNNISVVGSS DFCPPGHNTK KASYSGVSLF SNPVQYWEIQ PSTFRCVYVR SAIQLGNYK |
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| Overexpression of decorin in pancreatic cancer. A, expression of decorin mRNA in pancreatic tissues obtained from normal pancreas (n = 18) or pancreatic cancer patients (n = 44) was analyzed by real-time quantitative PCR. Individual data points represent the number of decorin copies per microliter of input cDNA, normalized to housekeeping genes hypoxanthine phosphoribosyltransferase and cyclophilin B. B, expression of decorin was analyzed in normal pancreas tissues (n = 6) and pancreatic cancer tissues (n = 6) by Western blot analysis. A representative blot is shown. Clinical Cancer Research Vol. 10, 4776-4783, July 15, 2004 | Immunohistochemical analysis of decorin in pancreatic tissue sections. A, normal pancreas. Weak decorin expression is seen in the connective tissue surrounding a small intralobular duct (d). Acinar cells, ductal cells, and islets (I, inset) do not express decorin. B–D, pancreatic cancer. B, the tumor cells (ca) do not express decorin and infiltrate a decorin-positive nerve (n). Intense decorin immunoreactivity is detected in the ECM around the neoplastic glands. C and D, higher magnification showing intense expression of decorin in the tumor ECM; the tumor cells (ca) are devoid of any decorin immunoreactivity. (D, inset) double immunohistochemistry showing that the actin-positive stellate cells exhibit a strong immunoreactivity for decorin and possibly represent the main source of the abundant expression of decorin in the ECM of pancreatic cancer tissues. Original magnification: x100, A and B; x200, C; x400, D. Clinical Cancer Research Vol. 10, 4776-4783, July 15, 2004 |
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| Standard Range: 31-2000 pg/ml | Standard Range: 15 - 1000 pg/ml |
| Sample required: 100 ul | Sample required: 100 ul |
| Sample Type: cell culture supernate, serum | Sample Type: cell culture supernate, serum |
| ELISA Name | Specice | Sample | Range |
Catalog No. | Quantity |
Price |
| Decorin ELISA Kit | human | cell culture supernate, serum | 32-2000 pg/ml |
PS001-42-EK-H-01 | 96 T |
450 |
| Decorin ELISA Kit | mouse | cell culture supernate | 16-1000 pg/ml |
PS001-42-EK-M-01 | 96 T |
450 |
| Antibody Name | Application | Specices | Host | Catalog No.: | Size |
Price |
| Decorin Antibody | WB, IHC | human | goat | PS001-42-AG-01 | 50 ug |
275 |
| Decorin Monoclonal Antibody | WB, IHC | human | mouse | PS001-42-MAG-01 | 50 ug |
240 |
| Recombinant Protein | Specice |
Expression Source |
Application |
Catalog No. | Quantity |
Price |
| Decorin, recombinant | human |
NS0 |
ELISA, BA |
PS001-42-RH-01-10 | 10 ug |
120 |
| Decorin, recombinant | mouse |
NS0 |
ELISA, BA |
PS001-42-RM-01-10 | 10 ug |
120 |
| Decorin overexpression reduces atherosclerosis development in apolipoprotein E-deficient mice |
| Atherosclerosis results from accumulation of macrophages and extracellular matrix in the arterial wall. Decorin, a small matrix proteoglycan, is able to regulate cell proliferation, migration and growth factors’ activity. We investigated the effect of decorin overexpression on atherosclerosis progression in apolipoprotein E-deficient (ApoE−/−) mice. Female ApoE−/− mice, 10 weeks old (early treatment, n=20) and 20 weeks old (delayed treatment, n=20) were administered intravenously with either an adenovirus (2.5×109 plaque-forming units/mouse) containing human decorin gene (Ad-Dcn) or β-galactosidase (LacZ), or PBS. Transgenic decorin was mainly expressed in the liver, and was secreted in the plasma up to 4 weeks. Six weeks after treatment, no significant difference in aortic root lesion size was observed between LacZ- and PBS-control groups. In contrast, Ad-Dcn-treated mice showed significantly reduced atherosclerotic lesions as compared to controls in both early and delayed treatment groups (2.9±1.1% versus 5.5±0.4%; p=0.004 and 13.4±1.3% versus 19.9±1.41%; p=0.009, respectively). In parallel, macrophage, gelatinase activity and collagen plaque content were also reduced. Interestingly, plasma triglycerides were reduced and decorin formed complexes with transforming growth factor-β1 (TGF-β1) that resulted in reduced circulating free-TGF-β1. |
| A . Al Haj Zen et al. Atherosclerosis , Volume 187 , Issue 1 , Pages 31 - 39 |
Decorin is a secreted protein associated with obesity and type 2 diabetes |
| expression in adipose tissue from normal glucose tolerant (NGT), impaired glucose tolerant and type 2 diabetic (T2D) Psammomys obesus. Adipose tissue was fractionated to determine which cells were responsible for decorin expression. The location of decorin protein expression in adipose tissue was determined using immunohistochemistry. Real-time PCR was used to measure decorin mRNA levels in human adipose tissue from 16 insulin-sensitive, 16 insulin-resistant and 6 T2D human subjects. Circulating plasma decorin concentrations were measured by enzyme-linked immunosorbent assay in 145 NGT and 141 T2D human individuals from a large-scale epidemiological study in Mauritius. RESULTS: Decorin mRNA was found to be highly expressed in adipose tissue, and decorin gene expression was significantly higher in visceral than that in subcutaneous adipose tissue depots in both P. obesus and human subjects (P=0.002 and P=0.001, respectively). Decorin mRNA was predominantly expressed by stromal/vascular cells of adipose tissue, and decorin protein in adipose tissue was primarily detected adjacent to blood vessels. Circulating plasma decorin levels in humans were elevated by 12% in T2D (P=0.049) compared to NGT subjects. There was a significant independent correlation between plasma decorin levels and waist-to-hip ratio (WHR, P=0.024). In male subjects, plasma decorin levels were significantly correlated with WHR (P=0.006), and fasting and 2-h glucose levels in an oral glucose tolerance test (P=0.027 and P=0.001, respectively). CONCLUSIONS: Decorin expression in adipose tissue was markedly upregulated in the obese state and may therefore play a role in adipose tissue homeostasis or in pathophysiology associated with obesity. |
Bolton K, et al. Int J Obes (Lond). 2008 Jul;32(7):1113-21. Epub 2008 Apr 15. |
An Antimetastatic Role for Decorin in Breast Cancer |
| Decorin, a member of the small leucine-rich proteoglycan gene family, down-regulates members of the ErbB receptor tyrosine kinase family and attenuates their signaling, leading to growth inhibition. We investigated the effects of decorin on the growth of ErbB2-overexpressing mammary carcinoma cells in comparison with AG879, an established ErbB2 kinase inhibitor. Cell proliferation and anchorage-independent growth assays showed that decorin was a potent inhibitor of breast cancer cell growth and a pro-apoptotic agent. When decorin and AG879 were used in combination, the inhibitory effect was synergistic in proliferation assays but only additive in both colony formation and apoptosis assays. Active recombinant human decorin protein core, AG879, or a combination of both was administered systemically to mice bearing orthotopic mammary carcinoma xenografts. Primary tumor growth and metabolism were reduced by approximately 50% by both decorin and AG879. However, no synergism was observed in vivo. Decorin specifically targeted the tumor cells and caused a significant reduction of ErbB2 levels in the tumor xenografts. Most importantly, systemic delivery of decorin prevented metastatic spreading to the lungs, as detected by novel species-specific DNA detection and quantitative assays. In contrast, AG879 failed to have any effect. Our data support a role for decorin as a powerful and effective therapeutic agent against breast cancer due to its inhibition of both primary tumor growth and metastatic spreading. |
| Goldoni S, et al. Am J Pathol. 2008 Aug 7. [Epub ahead of print] |
Decorin-mediated inhibition of proliferation and migration of the human trophoblast via different tyrosine kinase receptors |
Decorin (DCN), a decidua-derived TGF -binding proteoglycan, negatively regulates proliferation, migration and invasiveness of human extravillous trophoblast (EVT) cells in a TGF-independent manner. Present study examined underlying mechanisms, in particular possible roles of EGFR, IGFR-1 and VEGFR-2. EVT cell Sprouting from first trimester chorionic villus explants in the presence or absence of TGF-neutralizing antibody was inhibited with DCN, suggesting its negative regulatory role in situ. Inhibition of migration of the human EVT cell line HTR-8/SVneo in transwells undercoated with fibronectin was stronger when cells were briefly preincubated with DCN at 4°C (known to retard dissociation of receptor-ligand complex) than at 37°C, suggesting possible DCN action by cell membrane binding. Pretreatment of cells with an IGFR-1 blocking agent, but not two EGFR blocking agents or a VEGFR blocking agent significantly abrogated migration inhibitory effects of DCN, suggesting the involvement of IGFR-1 but not EGFR or VEGFR in migration inhibition by DCN. On the other hand, pretreatment with either of the EGFR blocking agents, or the VEGFR blocking agent but not the IGFR-1 blocking agent blocked proliferation inhibitory effects of DCN, indicating the roles of EGFR and VEGFR, but not IGFR-1 in antiproliferative action of DCN. EVT cells expressed EGFR, IGFR-1 and VEGFR-2. IGFR-1 and VEGF-R2 were phosphorylated in the presence of their natural ligands as well as DCN, and these events were blocked by pretreatment with respective receptor blocking agents indicating DCN-mediated activation of these receptors. In conclusion, DCN effects on EVT cells are mediated selectively by multiple tyrosine kinase receptors. |
D Iacob, et al. Endocrinology, doi:10.1210/en.2008-0780 |
Decorin suppresses lung metastases of murine osteosarcoma |
| Lung metastasis is the most crucial event affecting the therapeutic outcome of osteosarcoma. The prevention of lung metastasis is therefore important in improving the prognosis of patients with osteosarcoma. Decorin is a major extracellular matrix protein which has become the focus of various cancer studies. The biological role of decorin in osteosarcoma has yet to be clarified. The aim of this study was to examine the potential of decorin as a novel biological target for the treatment of osteosarcoma. In this study, the LM8 murine osteosarcoma cell line (LM8) with high metastatic potential to the lung was used. The two cell lines established were LM8-DCN which stably expressed human decorin (hDCN) and LM8-mock, established as a control. The LM8-DCN cell line was subcutaneously injected into the backs of mice. Significantly fewer pulmonary metastases were observed in mice with LM8-DCN compared to mice inoculated with LM8 and LM8-mock (P<0.001). In addition, the mice in the LM8-DCN inoculated group survived significantly longer than those in the LM8 and LM8-mock inoculated group, based on the Kaplan-Meier survival analysis and log-rank tests (P<0.005). The effect of decorin on the growth rates, motility and invasion ability of LM8 was investigated in vitro. There was no difference in the morphology and growth rates, but the motility and invasion of LM8 were inhibited by decorin. These results suggest that decorin has the therapeutic potential to prevent lung metastasis in osteosarcoma. |
Shintani K, et al. Oncol Rep. 2008 Jun;19(6):1533-9. |