ArticleBMC cancer2018
The expression of EMX2 lead to cell cycle arrest in glioblastoma cell line.
Article in BMC cancer, 2018. 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, 17 citations in OpenAlex.
- Addressing the Limits of Emx2 Therapy of Glioblastoma Multiforme by Transgene Insulation and Epigenetic Pharmacological Intervention.Biomedicines · 2026Article
- Empty Spiracles Homeobox 2 Transcription Factor Functions as a Tumor Suppressor in Renal Cell Carcinoma by Targeting CADM1.Molecular cancer research : MCR · 2025Article
- DNA methylation-activated full-length EMX1 facilitates metastasis through EMX1-EGFR-ERK axis in hepatocellular carcinoma.Cell death & disease · 2023Article
- EMX1 functions as a tumor inhibitor in spinal cord glioma through transcriptional suppression of WASF2 and inactivation of the Wnt/β-catenin axis.Brain and behavior · 2022Article
- Article
- Genetic Regulation of Vertebrate Forebrain Development by Homeobox Genes.Frontiers in neuroscience · 2022Review
- Functional New Transcription Factors (TFs) Associated with Cervical Cancer.Journal of healthcare engineering · 2022Article
- Construction of Prognostic Risk Model of Patients with Skin Cutaneous Melanoma Based on TCGA-SKCM Methylation Cohort.Computational and mathematical methods in medicine · 2022Article
- Empty spiracles homeobox genes EMX1 and EMX2 regulate WNT pathway activation in sarcomagenesis.Journal of experimental & clinical cancer research : CR · 2021Article
- Regulation of sarcomagenesis by the empty spiracles homeobox genes EMX1 and EMX2.Cell death & disease · 2021Article
- The Role of SVZ Stem Cells in Glioblastoma.Cancers · 2019Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastoma (GB) is a highly invasive primary brain tumor that nearly always systematically recurs at the site of resection despite aggressive radio-chemotherapy. Previously, we reported a gene expression signature related to tumor infiltration. Within this signature, the EMX2 gene encodes a homeodomain transcription factor that we found was down regulated in glioblastoma. As EMX2 is reported to play a role in carcinogenesis, we investigated the impact of EMX2 overexpression in glioma-related cell lines.
methodsFor that purpose, we constructed tetracycline-inducible EMX2 expression lines. Transfected cell phenotypes (proliferation, cell death and cell cycle) were assessed in time-course experiments.
resultsRestoration of EMX2 expression in U87 glioblastoma cells significantly inhibited cell proliferation. This inhibition was reversible after EMX2 removal from cells. EMX2-induced proliferative inhibition was very likely due to cell cycle arrest in G1/S transition and was not accompanied by signs of cell death.
conclusionOur results suggest that EMX2 may constitute a putative therapeutic target for GB treatment. Further studies are required to decipher the gene networks and transduction signals involved in EMX2's effect on cell proliferation.
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