ArticleEuropean journal of medical research2024
CD133 significance in glioblastoma development: in silico and in vitro study.
Article in European journal of medical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Low-Cost Self-Driven Liquid Biosensor Based on Metamaterials for Glioblastoma-Related Sample Detection.Biosensors · 2026Article
- MAGMAS Inhibition Enhances Temozolomide Efficacy in Chemotherapy-Resistant Glioblastoma Models.Cancer research communications · 2026Article
- The significance of epithelial-mesenchymal transition (EMT) in the initiation, plasticity, and treatment of glioblastoma.Genes & diseases · 2026Review
- Navigating the blood-brain barrier to blood-brain tumor barrier transition: microvascular P-glycoprotein and CD146 potentially contribute to glioma grading.Fluids and barriers of the CNS · 2025Article
- Vibrational spectroscopy unveils distinct cell cycle features of cancer stem cells in melanoma.Scientific reports · 2025Article
- The HOX Gene Family's Role as Prognostic and Diagnostic Biomarkers in Hematological and Solid Tumors.Cancers · 2025Review
- Unveiling the impact of CD133 on cell cycle regulation in radio- and chemo-resistance of cancer stem cells.Frontiers in public health · 2025Review
- The Original Mouse Models of Glioblastoma: Analysis of Pathophysiological Characteristics of Transplanted Tumor Tissue.Sovremennye tekhnologii v meditsine · 2025Article
- Article
- hsa-miR-181a-5p inhibits glioblastoma development via the MAPK pathway:Oncology research · 2024Article
- Article
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3 authors.
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Abstract
backgroundGlioblastoma multiform (GBM) is among the commonly diagnosed brain malignancies with poor prognosis. CD133 has been introduced as an oncogene in various cancers, like GBM. This study aimed to investigate the significance of CD133 in GBM development using in silico and in vitro techniques.
methodThe TCGA-GBM database was analyzed for the correlational and comparative studies. After selecting the U87MG cell line, CD133-siRNA was transfected into U87MG cells and treated with temozolomide. The cell viability, cell cycle, migration, clonogenicity, and apoptosis of groups were investigated using MTT, flow cytometry, wound-healing, colony formation, and annexin V/PI assays. Using qRT-PCR method, the mRNA expression levels of MMP16, SOX2, RAF1, MAP2K1, MAPK3, PIK3CA, AKT3, mTOR, CDK4, and BCL2 were studied.
resultsCD133 silencing improves apoptosis rate, arrests the cell cycle at the sub-G1 phase, suppresses the clonogenicity of U87MG cells, and inhibits the PI3K/Akt and MAPK pathways via downregulating the RAF1, MAP2K1, MAPK3, PIK3CA, AKT3, and mTOR expression. Besides, combining CD133 silencing with temozolomide treatment considerably inhibits the migration of U87MG cells compared to temozolomide monotherapy.
conclusionCD133 can regulate the PI3K/Akt and MAPK pathways and modulate the clonogenicity, apoptosis, and cell cycle of GBM. Combining CD133 silencing with temozolomide treatment considerably increases apoptosis, arrests the cell cycle at the sub-G1, and suppresses migration of U87MG cells compared to temozolomide monotherapy.
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