STC1 regulates glioblastoma migration and invasion via the TGF‑β/SMAD4 signaling pathway

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.

Targeting POLE2 Creates a Novel Vulnerability in Renal Cell Carcinoma via Modulating Stanniocalcin 1

“…It was pointed out in the literature that STC1 affected the occurrence and development of ovarian cancer ( Zhang et al, 2019 ), and could activate phosphorylation of Akt thereby affecting epithelial-mesenchymal transition (EMT) ( Yang et al, 2019 ). Besides, STC1 could affect the metastasis of glioma through the TGF-β/SMAD4 pathway ( Xiong and Wang, 2019 ), and affect the metastasis of liver cancer through the JNK pathway ( Chan et al, 2017 ). Some studied found that exogenous STC-1 could promote the RCC proliferation by reducing the levels of HIF-1α and Ca 2+ ( Zhu et al, 2014 ; Yang Q. et al, 2015 ).…”

Bioinformatics and Prediction Analysis of Long Non-coding RNAs in the Regulation of Glioblastoma Cell Migration and Invasion

“…promotes its progression through the WNT/β-catenin pathway 38 , and upregulation of SOX2 expression 39 . Our analysis predicts that NEAT1 affects SMAD4 and LOXL2, which were both established to be upregulated in GBM 40,41 . The miRNA miR124 was predicted to interact with NEAT1, and will subsequently target LOXL2, which also has been reported to target SMAD4 42 .…”

Development and Validation of a Hypoxia-Related Signature for Predicting Survival Outcomes in Patients With Bladder Cancer

“… Marie et al (2020) once conducted melanoblast transcriptome analysis and identified that the loss of KDELR3 could impair experimental metastasis. STC1 , a hypoxia-induced molecular target, could promote cell proliferations, invasion, migration, and metastasis in hepatocellular cancer, gastric cancer, colorectal cancer, breast cancer, and glioblastoma ( Chang et al, 2015 ; Rezapour et al, 2016 ; Chan et al, 2017 ; Wang Y. et al, 2019 ; Xiong and Wang, 2019 ). With the exception of Jun, the remaining seven genes have not been studied in bladder cancer to date, but their ability to promote or weaken malignant phenotypes was well presented in our signature.…”