ArticleInternational journal of molecular sciences2014
Int6/eIF3e is essential for proliferation and survival of human glioblastoma cells.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 39 citations in OpenAlex.
- eIF3e-mediated translational checkpoint maintains immune tolerance and prevents lymphoid malignancy.The Journal of experimental medicine · 2026Article
- eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by small molecules.Cell reports · 2025Article
- eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by novel small molecules.bioRxiv : the preprint server for biology · 2025Article
- Preclinical approach of two novel tetrahydroquinoline derivatives targeting GPER and Bcl-2 for anti-glioblastoma therapy.Scientific reports · 2025Article
- Understanding the Significance of Hypoxia-Inducible Factors (HIFs) in Glioblastoma: A Systematic Review.Cancers · 2024Review
- Decreased eukaryotic initiation factors expression upon temozolomide treatment-potential novel implications for eIFs in glioma therapy.Journal of neuro-oncology · 2023Article
- Cellular Exposure to Chloroacetanilide Herbicides Induces Distinct Protein Destabilization Profiles.ACS chemical biology · 2023Article
- Expression pattern, tumor immune landscape, and prognostic value of N7‑methylguanosine regulators in bladder urothelial carcinoma.Oncology letters · 2023Article
- The dark side of mRNA translation and the translation machinery in glioblastoma.Frontiers in cell and developmental biology · 2023Review
- Comparative proteomic analysis identifies differentially expressed proteins and reveals potential mechanisms of traumatic heterotopic ossification progression.Journal of orthopaedic translation · 2022Article
- The Roles and Regulation of mBiomedicines · 2022Review
- Translational Regulation by hnRNP H/F Is Essential for the Proliferation and Survival of Glioblastoma.Cancers · 2022Article
- Article
- Translation reprogramming by eIF3 linked to glioblastoma resistance.NAR cancer · 2020Article
- Genetic Profiles Playing Opposite Roles of Pathogenesis in Schizophrenia and Glioma.Journal of oncology · 2020Article
- Relevance of Translation Initiation in Diffuse Glioma Biology and its Therapeutic Potential.Cells · 2019Review
- Array Comparative Genomic Hybridization Analysis Reveals Significantly Enriched Pathways in Canine Oral Melanoma.Frontiers in oncology · 2019Article
- Eukaryotic translation initiation factor 3 (eIF3) subunit e is essential for embryonic development and cell proliferation.FEBS open bio · 2018Article
- Article
- Up-regulation Of EIF3e Is Associated with The Progression of Esophageal Squamous Cell Carcinoma and Poor Prognosis in Patients.Journal of Cancer · 2018Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastomas (GBM) are very aggressive and malignant brain tumors, with frequent relapses despite an appropriate treatment combining surgery, chemotherapy and radiotherapy. In GBM, hypoxia is a characteristic feature and activation of Hypoxia Inducible Factors (HIF-1α and HIF-2α) has been associated with resistance to anti-cancer therapeutics. Int6, also named eIF3e, is the "e" subunit of the translation initiation factor eIF3, and was identified as novel regulator of HIF-2α. Eukaryotic initiation factors (eIFs) are key factors regulating total protein synthesis, which controls cell growth, size and proliferation. The functional significance of Int6 and the effect of Int6/EIF3E gene silencing on human brain GBM has not yet been described and its role on the HIFs is unknown in glioma cells. In the present study, we show that Int6/eIF3e suppression affects cell proliferation, cell cycle and apoptosis of various GBM cells. We highlight that Int6 inhibition induces a diminution of proliferation through cell cycle arrest and increased apoptosis. Surprisingly, these phenotypes are independent of global cell translation inhibition and are accompanied by decreased HIF expression when Int6 is silenced. In conclusion, we demonstrate here that Int6/eIF3e is essential for proliferation and survival of GBM cells, presumably through modulation of the HIFs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.