ArticleCommunications biology2022
Iron commensalism of mesenchymal glioblastoma promotes ferroptosis susceptibility upon dopamine treatment.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- GPR40 Attenuates Glioma TMZ-Resistance Through Ferroptosis Inhibition.Neurochemical research · 2026Article
- Icaritin inhibits breast cancer through activating MT1X to promote ferroptosis and synergizing with NF-κB pathway suppression.Frontiers in oncology · 2026Article
- Harnessing ferroptosis to transform glioblastoma therapy and surmount treatment resistance.Cell death discovery · 2025Review
- Iron Mediates Radiation-Induced Glioblastoma Cell Diffusion.International journal of molecular sciences · 2025Article
- Targeting metabolic reprogramming in glioblastoma as a new strategy to overcome therapy resistance.Frontiers in cell and developmental biology · 2025Review
- Mitochondrial Iron Metabolism as a Potential Key Mediator of PD-L1 Thermal Regulation.Cancers · 2024Article
- Navigating glioblastoma complexity: the interplay of neurotransmitters and chromatin.Molecular biology reports · 2024Review
- Humanin activates integrin αV-TGFβ axis and leads to glioblastoma progression.Cell death & disease · 2024Article
- Crosstalk between glioblastoma and tumor microenvironment drives proneural-mesenchymal transition through ligand-receptor interactions.Genes & diseases · 2024Review
- A closer look at the role of iron in glioblastoma.Neuro-oncology · 2023Review
- Autophagy-dependent ferroptosis as a potential treatment for glioblastoma.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The heterogeneity of glioblastoma multiforme (GBM) leads to poor patient prognosis. Here, we aim to investigate the mechanism through which GBM heterogeneity is coordinated to promote tumor progression. We find that proneural (PN)-GBM stem cells (GSCs) secreted dopamine (DA) and transferrin (TF), inducing the proliferation of mesenchymal (MES)-GSCs and enhancing their susceptibility toward ferroptosis. PN-GSC-derived TF stimulates MES-GSC proliferation in an iron-dependent manner. DA acts in an autocrine on PN-GSC growth in a DA receptor D1-dependent manner, while in a paracrine it induces TF receptor 1 expression in MES-GSCs to assist iron uptake and thus enhance ferroptotic vulnerability. Analysis of public datasets reveals worse prognosis of patients with heterogeneous GBM with high iron uptake than those with other GBM subtypes. Collectively, the findings here provide evidence of commensalism symbiosis that causes MES-GSCs to become iron-addicted, which in turn provides a rationale for targeting ferroptosis to treat resistant MES GBM.
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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.