We are analyzing https://link.springer.com/article/10.1007/s00109-008-0414-3.

Title:
Transferrin-receptor-mediated iron accumulation controls proliferation and glutamate release in glioma cells | Journal of Molecular Medicine
Description:
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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Keywords {🔍}

article, google, scholar, pubmed, cas, cell, proliferation, cancer, iron, glioma, cells, molecular, expression, ets, glutamate, tfr, signaling, access, receptor, nat, germany, transferrin, brain, human, tumor, growth, biol, rev, berlin, privacy, cookies, content, journal, medicine, accumulation, promotes, mol, med, information, publish, research, search, release, markovic, chiarugi, meier, glass, transcription, lines, protein,

Topics {✒️}

caused n-methyl-d-aspartate-receptor-mediated reduction ets transcription factors month download article/chapter oxidatively modified proteins protein tyrosine phosphatase transferrin receptor gene cell cycle-dependent inhibition urokinase-type plasminogen activator sonderforschungsbereich grant tr3/b5 promotes glioma proliferation reduces calcium-dependent apoptosis malignant potential akt/nf-kappab signaling oxidative stress ets-1 proto-oncogene correlates protein-tyrosine phosphatases transferrin receptor glioma cell proliferation hif-1alpha accumulation related subjects full article pdf high-grade glioma neoplastic brain tissue reactive oxidant signaling privacy choices/manage cookies molecular medicine aims serum-free culture brain-tumor immunotherapy lung adenocarcinoma cells akt-induced phosphorylation signaling pathways involved prostate cancer cells neuron cell mass free radical induction check access instant access mechanism providing space mitochondrial dysfunction creatine kinase bb 2/neu-overexpressing cells forced tfr expression malignant gliomas cyclin-dependent kinases integrin alpha5 expression human astrocytic tumors redox-based switch subsequent rb phosphorylation cell growth inhibition progressing tumor mass european economic area

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         headline:Transferrin-receptor-mediated iron accumulation controls proliferation and glutamate release in glioma cells
         description: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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      headline:Transferrin-receptor-mediated iron accumulation controls proliferation and glutamate release in glioma cells
      description: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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         ETS
         Free radicals
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         Molecular Medicine
         Human Genetics
         Internal Medicine
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