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Objective:To investigate the expression of stanniocalcin-2 (STC-2) and cellular-mesenchymal epithelial transition factor (C-met) in tumor tissues of cervical cancer patients and their clinical significance.Methods:A total of 110 cervical cancer patients were selected in Foshan First People′s Hospital from January 2014 to December 2018. Patients′ cancer tissue samples and normal tissue samples were collected during modified radical resection to determine and compare the expression levels of STC-2 mRNA and C-met mRNA in the two tissues, and to analyze the correlation between the expression levels of STC-2, C-met and the clinicopathological characteristics of the patients as well as the multivariate analysis of tumor metastasis and recurrence in the patients. The correlation between the expression of STC-2 and C-met and the time of postoperative tumor metastasis and recurrence in cervical cancer patients were analyzed after 24 months of follow-up.Results:The expression levels of C-met mRNA and STC-2 mRNA in cancer tissues were higher than those in adjacent normal tissues: 4.51 ± 1.21 vs. 3.97 ± 1.14, 2.57 ± 0.21 vs. 2.12 ± 0.24, there were statistical differences ( t = 3.41, 14.80, P<0.05). The expression of STC-2 and C-met in cancer tissues had no significant difference with age, pathological type, federation international of gynecology and obstetrics (FIGO) stage and tumor size ( P>0.05), but had significant difference with tumor recurrence or metastasis ( P<0.05). The results of Logistic multivariate analysis showed that vascular emboli, lymph node metastasis, TNM stage, depth of tumor invasion, C-met expression and STC-2 expression were independent risk factors affecting the prognosis of cervical cancer patients ( P<0.05). The expression of STC-2 and C-met were negatively correlated with the time of tumor metastasis in patients with cervical cancer ( r = - 0.663, P<0.001; r = - 0.747, P<0.001). Conclusions:The expression levels of STC-2 and C-met in cancer tissues of cervical cancer patients are higher than those in adjacent normal tissues, and the expression levels of STC-2 and C-met are negatively correlated with the time of metastasis. The expression of C-met, the expression of STC-2, vascular emboli, lymph node metastasis, TNM stage, and the depth of tumor invasion are all independent risk factors affecting the prognosis of cervical cancer patients.
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Stanniocalcin 2,a secreted glycoprotein hormone,has been found to be highly expressed in a variety of human malignancies.Through several signal transdution pathways,stanniocalcin 2 plays important roles in the regulation of many biological events of tumor such as proliferation,apoptosis,invasion and metastasis,hypoxia tolerating and drug resistance,indicating stanniocalcin 2 may be a pivotal node in the molecular regulation network of tumor.Stanniocalcin 2 is expected to become a novel biomarker and therapeutic target for diagnosis and treatment of tumor if the funtional mechanisms of stanniocalcin 2 could be further elaborated.
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Objective To study the effect of STC2 on invasion and metastasis of breast cancer cells and its mechanism.Methods By 231 HM shRNA interference cell STC2,we observed fiber cells expressing form,number plate cloning experiment statistical analysis.Immune co-precipitation (CO-IP) for testing related protein expression.Results By 231 HM STC2 cells expressing shRNA interference,231 HM presents high transfer characteristics of fiber cell morphology,cell invasion and metastasis ability of increase at the same time;On the contrary,after 231 cells expressing STC2,cell invasion and metastasis ability induced.In addition,after reducing STC2 expression of 231 HM cells,its resistance to radiation-inducled apoptosis and expression of STC2 after 231 reduced,ability to resist radiation induced apoptosis of cells induled too.Conclusion Collectively,these results indicate that STC2 may inhibit EMT at least partially through the PKC/Claudin-1-mediated signaling in human breast cancer cells.
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AIM:To explore the effects of stanniocalcin 2 (STC2) on the proliferation, migration and the process of epithelial-mesenchymal transition (EMT) in human hepatocellular carcinoma HepG2 cells.METHODS:The expression levels of STC2 in the hepatocellular carcinoma cell lines and normal liver cells were assessed by Western blot.Colony formation assay was used to test the effect of STC2 on the proliferation of HepG2 cells.The effects of STC2 on the expression of proliferation-related molecules at mRNA and protein levels were determined by RT-qPCR and Western blot.The effect of STC2 on the migration ability was measured by Transwell assay.The mRNA and protein levels of vimentin and E-cadherin in STC2-overexpressing and-silencing cell lines were detected by RT-qPCR and Western blot.RESULTS:Compared with the normal liver cell line, the protein expression of STC2 was up-regulated in the hepatocellular carcinoma cell lines.The results of colony formation assay indicated that STC2 promoted the proliferation of HepG2 cells.STC2 significantly regulated the proliferation-related gene expression, such as cyclin D1.The results of Transwell assay showed that STC2 enhanced the migration ability of the HepG2 cells and influenced the EMT process.CONCLUSION:STC2 promotes the proliferation of HepG2 cells and affects the expression of proliferation-related genes.STC2 influences the process of EMT and promotes the migration of HepG2 cells.
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Aims: The acquired cholesteatoma, even with all the knowledge accumulated since its first description, still remains a public health problem, far from being solved. A deeper understanding of its pathogenesis is extremely important since it is a destructive lesion that might cause potentially serious complications. We had the objective, in this study, to identify acquired cholesteatoma biomarkers using proteomics platform. Study Design: descriptive cross-sectional study. Methodology: Samples were collected from cholesteatoma and also from the retroauricular skin of twelve patients undergoing surgery for cholesteatoma removal. The samples were studied by proteomic analysis, using the Mascot algorithm and the NCBI and Swiss Prot proteins database. Results: Of the 393 spots identified in the analysis of protein extracts of acquired cholesteatoma, only 10 were within acceptable statistical parameters by Mascot algorithm. The proteins detected in acquired cholesteatoma were fibrinogen beta chain, extracellular matrix protein 2, actin cytoplasmic 1, heparan sulfate glucosamine 3-O-sulfotransferase 3A1, tumor necrosis factor alpha 8 induced protein-like 1, stanniocalcin-2, eosinophil lysophospholipase and OFUT1. Conclusion: Proteins involved in cell migration, regulation of apoptosis, signaling pathways, cellular proliferation, wound healing and inflammatory processes were identified. We were able to draw a proteomic profile of acquired cholesteatoma.
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OBJECTIVE: Stanniocalcin 2 (STC2) is a glycoprotein hormone that is widely expressed in mammalian kidney, heart, and thymus. However, the potential function of STC2 in the brain is less understood. In this study, we investigated whether treatment with STC2 influenced cell proliferation and neurogenesis in imprinting control region (ICR) mice. METHODS: 100 nM STC2 and 5'-bromo-2'-deoxyuridine (BrdU) (50 mg/kg) were administered intracerebroventricularly and intraperitoneally, respectively. On days 1 and 21 after the BrdU injection, sections of STC2-treated group and controls were carried out immunohistochemistry using anti-BrdU and anti-phosphor-cAMP-response element-binding protein (CREB) antibody. RESULTS: We found that the number of BrdU-positive cells was significantly increased in the hippocampal dentate gyrus (DG), compared with controls. Next, we observed that CREB phosphorylation was decreased in the hippocampal DG of STC2-treated group versus the controls. CONCLUSION: These results suggest that STC2 treatment may increase cell proliferation by increasing CREB phosphorylation in the subgranular zone of the DG.