ArticleJournal of molecular medicine (Berlin, Germany)2009
Transferrin-receptor-mediated iron accumulation controls proliferation and glutamate release in glioma cells.
Article in Journal of molecular medicine (Berlin, Germany), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Value of Ferritin Heavy Chain (FTH1) Expression in Diagnosis and Prognosis of Renal Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2019Pooled it
- SIRT5-mediated BCAT1 desuccinylation and stabilization leads to ferroptosis insensitivity and promotes cell proliferation in glioma.Cell death & disease · 2025Article
- Identification and Characterization of Oxidative Stress and Endoplasmic Reticulum Stress-Related Genes in Esophageal Cancer.Journal of Cancer · 2025Article
- Differentiation and Growth-Arrest-Related lncRNA (International journal of molecular sciences · 2024Article
- High expression of BCAT1 sensitizes AML cells to PARP inhibitor by suppressing DNA damage response.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Article
- Antisense-oligonucleotide co-micelles with tumor targeting peptides elicit therapeutic effects by inhibiting microRNA-21 in the glioblastoma animal models.Journal of advanced research · 2023Article
- PotentFrontiers in oncology · 2023Article
- Ferroptosis and PPAR-gamma in the limelight of brain tumors and edema.Frontiers in oncology · 2023Review
- NUF2 Drives Cholangiocarcinoma Progression and Migration via Inhibiting Autophagic Degradation of TFR1.International journal of biological sciences · 2023Article
- SCARA5 induced ferroptosis to effect ESCC proliferation and metastasis by combining with Ferritin light chain.BMC cancer · 2022Article
- A role for ceruloplasmin in the control of human glioblastoma cell responses to radiation.BMC cancer · 2022Article
- Correlation of Ferroptosis and Other Types of Cell Death in Neurodegenerative Diseases.Neuroscience bulletin · 2022Review
- Altered Elemental Distribution in Male Rat Brain Tissue as a Predictor of Glioblastoma Multiforme Growth-Studies Using SR-XRF Microscopy.International journal of molecular sciences · 2022Article
- Emerging roles of ferroptosis in glioma.Frontiers in oncology · 2022Review
- Article
- Identification of Iron Metabolism-Related Genes as Prognostic Indicators for Lower-Grade Glioma.Frontiers in oncology · 2021Article
- Alterations in Cellular Iron Metabolism Provide More Therapeutic Opportunities for Cancer.International journal of molecular sciences · 2018Review
- Transferrin receptor 1 in cancer: a new sight for cancer therapy.American journal of cancer research · 2018Review
- RNA Editing-Systemic Relevance and Clue to Disease Mechanisms?Frontiers in molecular neuroscience · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transferrin receptors (TfR) are overexpressed in brain tumors, but the pathological relevance has not been fully explored. Here, we show that TfR is an important downstream effector of ets transcription factors that promotes glioma proliferation and increases glioma-evoked neuronal death. TfR mediates iron accumulation and reactive oxygen formation and thereby enhanced proliferation in clonal human glioma lines, as shown by the following experiments: (1) downregulating TfR expression reduced proliferation in vitro and in vivo; (2) forced TfR expression in low-grade glioma accelerated proliferation to the level of high-grade glioma; (3) iron and oxidant chelators attenuated tumor proliferation in vitro and tumor size in vivo. TfR-induced oxidant accumulation modified cellular signaling by inactivating a protein tyrosine phosphatase (low-molecular-weight protein tyrosine phosphatase), activating mitogen-activated protein kinase and Akt and by inactivating p21/cdkn1a and pRB. Inactivation of these cell cycle regulators facilitated S-phase entry. Besides its effect on proliferation, TfR also boosted glutamate release, which caused N-methyl-D-aspartate-receptor-mediated reduction of neuron cell mass. Our results indicate that TfR promotes glioma progression by two mechanisms, an increase in proliferation rate and glutamate production, the latter mechanism providing space for the progressing tumor mass.
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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.