Stanniocalcin-1 (STc1) is involved in cancer progression; however, the function of STc1 in glioblastoma remains unknown. in the present study, the expression levels of STc1 protein in glioblastoma were detected using immunohistochemistry. The expression levels of STc1, SMad2/3 and SMad4 proteins, following silencing of STc1, were assessed via western blotting. edu and Transwell assays were performed to determine the proliferation and migration ability of the cells. The mrna expression levels of STc1, SMad4 and microrna (mir)-34a were determined using quantitative Pcr. The expression levels of STc1 were increased in glioblastoma tissues. STc1 revealed a significant association with poor outcome in patients with glioblastoma (P<0.05). The proliferation and invasion abilities were repressed in ln229 cells infected with lV3-shSTc1-1 and lV3-shSTc1-2 compared with lV3-nc. By contrast, the proliferation and invasion abilities were increased in T98G cells infected with lV5-STc1 compared with lV5-nc (P<0.05). The expression levels of STc1, SMad2/3 and SMad4 were decreased in ln229 cells infected with lV3-shSTc1-1 and lV3-shSTc1-2 compared with lV3-nc. However, the expression levels of STc1, SMad2/3 and SMad4 were elevated in T98G cells infected with lV5-STc1 compared with lV5-nc. The expression levels of mir-34a were decreased following silencing of STc1 (P<0.05). The expression levels of SMad4 were decreased when transfected with mir-34a mimics (P<0.05). The luciferase activity of the wild-type 3'untranslated region of SMad4 was decreased following transfection with mir-34a mimics (P<0.05). Silencing of STc1 inhibited the growth of ln229 in vivo. in conclusion, STc1 expression levels were increased in the present study, and it was revealed that STc1 regulated glioblastoma malignancy. This phenotype was observed in the SMad2/3 and SMad4 pathways.
LINC00675 has been suggested to be dysregulated in gastric cancer, colorectal cancer and pancreatic cancer. However, the expression status and biological function of LINC00675 in glioma were still unknown. Thus, we reported LINC00675 was overexpressed in glioma tissues and cell lines, and positively associated with advanced WHO grade, large tumor size and poor prognosis. Moreover, univariate and multivariate analyses suggested that high-expression of LINC00675 was an independent unfavorable prognostic predictor for glioma. In addition, levels of LINC00675 expression were positively correlated with TRIP6 mRNA and protein expressions. The in vitro experiment showed that silencing of LINC00675 inhibits glioma cell proliferation, migration and invasion through regulating TRIP6. In conclusion, LINC00675 acts as a tumor promoter in glioma progression.
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