ArticleMolecular medicine reports2019
FOXC1 silencing inhibits the epithelial‑to‑mesenchymal transition of glioma cells: Involvement of β‑catenin signaling.
Article in Molecular medicine reports, 2019. 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, 19 citations in OpenAlex.
- Article
- FOXC1 as a molecular predictor of postoperative peritumoral edema resolution in meningiomas.Journal of neuro-oncology · 2026Article
- Construction of an actin cytoskeleton-related gene signature for predicting prognosis and therapeutic response in glioblastoma: based on machine learning.Translational cancer research · 2026Article
- FOXC1 expression and radiological predictors of peritumoral brain edema in meningiomas.Journal of neuro-oncology · 2026Article
- The Role of Epithelial-Mesenchymal Transition in Osteosarcoma Progression: From Biology to Therapy.Diagnostics (Basel, Switzerland) · 2025Review
- BPTF promotes glioma development through USP34-mediated de-ubiquitination of FOXC1.Histology and histopathology · 2025Article
- Reciprocal regulation of forkhead box C1 and L1 cell adhesion molecule contributes to triple-negative breast cancer progression.Breast cancer research and treatment · 2024Article
- FOXC2 Promotes Vasculogenic Mimicry in Ovarian Cancer.Cancers · 2022Article
- FOXC1‑mediated TRIM22 regulates the excessive proliferation and inflammation of fibroblast‑like synoviocytes in rheumatoid arthritis via NF‑κB signaling pathway.Molecular medicine reports · 2022Article
- Overexpression of FOXC1 Promotes Tumor Metastasis by Activating the Wnt/β-Catenin Signaling Pathway in Gastric Cancer.Digestive diseases and sciences · 2022Article
- Recognition of a Novel Gene Signature for Human Glioblastoma.International journal of molecular sciences · 2022Article
- Overexpression of Foxc1 ameliorates sepsis‑associated encephalopathy by inhibiting microglial migration and neuroinflammation through the IκBα/NF‑κB pathway.Molecular medicine reports · 2022Article
- Epithelial-mesenchymal transition and its transcription factors.Bioscience reports · 2022Review
- PRL1 Promotes Glioblastoma Invasion and TumorigenesisFrontiers in oncology · 2021Article
- Therapeutically Targeting Cancers That Overexpress FOXC1: A Transcriptional Driver of Cell Plasticity, Partial EMT, and Cancer Metastasis.Frontiers in oncology · 2021Review
- Identification of low-dose radiation-induced exosomal circ-METRN and miR-4709-3p/GRB14/PDGFRα pathway as a key regulatory mechanism in Glioblastoma progression and radioresistance: Functional validation and clinical theranostic significance.International journal of biological sciences · 2021Article
- Overexpression of Foxc1 regenerates crushed rat facial nerves by promoting Schwann cells migration via the Wnt/β-catenin signaling pathway.Journal of cellular physiology · 2020Article
- MIR-138-5P inhibits the progression of prostate cancer by targeting FOXC1.Molecular genetics & genomic medicine · 2020Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioma is a type of malignant brain tumor. Forkhead box C1 (FOXC1) is a conserved transcription factor that is involved in tumorigenesis; however, the function of FOXC1 in glioma remains unclear. The present study aimed to investigate the effects of FOXC1 silencing on the epithelial‑to‑mesenchymal transition (EMT) of glioma cells. FOXC1‑specific small interfering RNAs were employed to downregulate the expression levels of FOXC1 in glioma cells. The proliferation, migration and invasion of glioma cells were assessed by MTT assay, wound healing assay and Transwell assay. Western blot analysis was performed to reveal the effects of FOXC1 on EMT‑associated proteins and β‑catenin signaling. The results revealed that, following FOXC1 silencing, the proliferation, migration and invasion of glioma cells were decreased. The expression levels of EMT‑associated proteins were also affected. Further examination demonstrated that β‑catenin signaling was involved in the effects of FOXC1 on glioma cells. Previous results suggested that overexpression of β‑catenin reversed the effects of FOXC1 silencing on glioma cells. The present study demonstrated that FOXC1 may regulate the EMT of glioma cells, potentially via β‑catenin signaling. Therefore, FOXC1 may be a potential therapeutic target for the treatment of glioma.
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Registered trials
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