ArticleCell death & disease2011
Frataxin participates to the hypoxia-induced response in tumors.
Article in Cell death & disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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.
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Who cites it
30 citing papers in PubMed, 56 citations in OpenAlex.
- FXN predicts poor prognosis in colon adenocarcinoma and correlates with immune cell infiltration.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- The Molecular Interplay Between p53-Mediated Ferroptosis and Non-Coding RNAs in Cancer.International journal of molecular sciences · 2025Review
- Frataxin: from the sequence to the biological role.Biophysical reviews · 2025Review
- An RNA-seq study in Friedreich ataxia patients identified hsa-miR-148a-3p as a putative prognostic biomarker of the disease.Human genomics · 2024Article
- MRPS16 promotes lung adenocarcinoma growth via the PI3K/AKT/Frataxin signalling axis.Journal of cellular and molecular medicine · 2024Article
- CAGI, the Critical Assessment of Genome Interpretation, establishes progress and prospects for computational genetic variant interpretation methods.Genome biology · 2024Article
- Targeting Iron-Sulfur Clusters in Cancer: Opportunities and Challenges for Ferroptosis-Based Therapy.Cancers · 2023Review
- Dimorphic frataxin and its gene regulation by sex steroids in hamsters.Molecular genetics and genomics : MGG · 2023Article
- Loss of filamentous actin, tight junction protein expression, and paracellular barrier integrity in frataxin-deficient human brain microvascular endothelial cells-implications for blood-brain barrier physiology in Friedreich's ataxia.Frontiers in molecular biosciences · 2023Article
- Adaptive Changes Allow Targeting of Ferroptosis for Glioma Treatment.Cellular and molecular neurobiology · 2022Review
- Iron-Sulfur Clusters: A Key Factor of Regulated Cell Death in Cancer.Oxidative medicine and cellular longevity · 2022Review
- Recent Advances in the Elucidation of Frataxin Biochemical Function Open Novel Perspectives for the Treatment of Friedreich's Ataxia.Frontiers in neuroscience · 2022Review
- Drug Repositioning in Friedreich Ataxia.Frontiers in neuroscience · 2022Review
- Iron-Sulfur Cluster Biogenesis as a Critical Target in Cancer.Antioxidants (Basel, Switzerland) · 2021Review
- Analysis and Interpretation of the Impact of Missense Variants in Cancer.International journal of molecular sciences · 2021Review
- Iron: An Essential Element of Cancer Metabolism.Cells · 2020Review
- Metabolic host response and therapeutic approaches to influenza infection.Cellular & molecular biology letters · 2020Review
- Evaluating the predictions of the protein stability change upon single amino acid substitutions for the FXN CAGI5 challenge.Human mutation · 2019Article
- Characterization of human frataxin missense variants in cancer tissues.Human mutation · 2019Article
- Linking Cancer Metabolic Dysfunction and Genetic Instability through the Lens of Iron Metabolism.Cancers · 2019Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
Defective expression of frataxin is responsible for the degenerative disease Friedreich's ataxia. Frataxin is a protein required for cell survival since complete knockout is lethal. Frataxin protects tumor cells against oxidative stress and apoptosis but also acts as a tumor suppressor. The molecular bases of this apparent paradox are missing. We therefore sought to investigate the pathways through which frataxin enhances stress resistance in tumor cells. We found that frataxin expression is upregulated in several tumor cell lines in response to hypoxic stress, a condition often associated with tumor progression. Moreover, frataxin upregulation in response to hypoxia is dependent on hypoxia-inducible factors expression and modulates the activation of the tumor-suppressor p53. Importantly, we show for the first time that frataxin is in fact increased in human tumors in vivo. These results show that frataxin participates to the hypoxia-induced stress response in tumors, thus implying that modulation of its expression could have a critical role in tumor cell survival and/or progression.
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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.