ArticleInternational journal of oncology2017
The mechanism of epithelial-mesenchymal transition induced by TGF-β1 in neuroblastoma cells.
Article in International journal of oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Smad4 regulates TGF-β1-mediated hedgehog activation to promote epithelial-to-mesenchymal transition in pancreatic cancer cells by suppressing Gli1 activity.Computational and structural biotechnology journal · 2024Article
- Article
- Copper chelation suppresses epithelial-mesenchymal transition by inhibition of canonical and non-canonical TGF-β signaling pathways in cancer.Cell & bioscience · 2023Article
- Prognostic significance of NT5E/CD73 in neuroblastoma and its function in CSC stemness maintenance.Cell biology and toxicology · 2023Article
- Inhibition of Cell Proliferation and Metastasis by Scutellarein Regulating PI3K/Akt/NF-κB Signaling through PTEN Activation in Hepatocellular Carcinoma.International journal of molecular sciences · 2021Article
- Mesenchymal Stromal Cells in Neuroblastoma: Exploring Crosstalk and Therapeutic Implications.Stem cells and development · 2021Review
- Multiomics Analysis of Neuroblastoma Cells Reveals a Diversity of Malignant Transformations.Frontiers in cell and developmental biology · 2021Article
- Tumor-associated macrophages promote human hepatoma Huh-7 cell migration and invasion through the Gli2/IGF-II/ERK1/2 axis by secreting TGF-β1.Cancer biology & therapy · 2020Article
- Mesenchymal Transformation: The Rosetta Stone of Glioblastoma Pathogenesis and Therapy Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Review
- EDIL3 regulates gastric cancer cell migration, invasion and epithelial-mesenchymal transition via TGF-β1/XIST/miR-137 feedback loop.Translational cancer research · 2020Article
- Downregulation of uPAR promotes urokinase translocation into the nucleus and epithelial to mesenchymal transition in neuroblastoma.Journal of cellular physiology · 2020Article
- Article
- Innate and Adaptive Immunity Linked to Recognition of Antigens Shared by Neural Crest-Derived Tumors.Cancers · 2020Review
- Article
- Regulating autophagy facilitated therapeutic efficacy of the sonic Hedgehog pathway inhibition on lung adenocarcinoma through GLI2 suppression and ROS production.Cell death & disease · 2019Article
- Influence of SHH/GLI1 axis on EMT mediated migration and invasion of breast cancer cells.Scientific reports · 2019Article
- Natural Killer-Derived Exosomal miR-186 Inhibits Neuroblastoma Growth and Immune Escape Mechanisms.Cancer research · 2019Article
- Paeoniflorin Inhibits Migration and Invasion of Human Glioblastoma Cells via Suppression Transforming Growth Factor β-Induced Epithelial-Mesenchymal Transition.Neurochemical research · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroblastoma is the second most common extracranial malignant solid tumor that occurs in childhood, and metastasis is one of the major causes of death in neuroblastoma patients. The epithelial-mesenchymal transition (EMT) is an important mechanism for both the initiation of tumor invasion and subsequent metastasis. Therefore, this study investigated the mechanism by which transforming growth factor (TGF)-β1 induces EMT in human neuroblastoma cells. Using quantitative RT-qPCR and western blot analyses, we found that the mRNA and protein expression levels of E-cadherin were significantly decreased, whereas that of α-SMA was significantly increased after neuroblastoma cells were treated with different concentrations of TGF-β1. A scratch test and Transwell migration assay revealed that cell migration significantly and directly correlated with the concentration of TGF-β1 indicating that TGF-β1 induced EMT in neuroblastoma cells and led to their migration. Inhibiting Smad2/3 expression did not affect the expression of the key molecules involved in EMT. Further investigation found that the expression of the glioblastoma transcription factor (Gli) significantly increased in TGF-β1-stimulated neuroblastoma cells undergoing EMT, accordingly, interfering with Gli1/2 expression inhibited TGF-β1-induced EMT in neuroblastoma cells. GANT61, which is a targeted inhibitor of Gli1 and Gli2, decreased cell viability and promoted cell apoptosis. Thus, TGF-β1 induced EMT in neuroblastoma cells to increase their migration. Specifically, EMT induced by TGF-β1 in neuroblastoma cells did not depend on the Smad signaling pathway, and the transcription factor Gli participated in TGF-β1-induced EMT independent of Smad signaling.
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