STC1 regulates glioblastoma migration and invasion via the TGF??/SMAD4 signaling pathway.
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ABSTRACT: 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.
SUBMITTER: Xiong Y
PROVIDER: S-EPMC6755173 | biostudies-literature | 2019 Oct
REPOSITORIES: biostudies-literature
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