ReviewInternational journal of molecular sciences2023
Ferroptosis, Metabolic Rewiring, and Endometrial Cancer.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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
18 citing papers in PubMed, 22 citations in OpenAlex.
- Subtype-specific mechanisms of lipid metabolism in gynecological malignancies and novel targeted intervention strategies (Review).Oncology letters · 2026Review
- GOT1 promotes endometrial cancer progression by regulating ferroptosis through the STAT3-GPX4 axis and attenuating medroxyprogesterone acetate sensitivity.Cancer gene therapy · 2026Article
- Doxorubicin induces ferroptosis in endometrial cancer by suppressing the MKK6/p38/CEBPB axis.Journal of translational medicine · 2026Article
- Oxidative stress as a nexus: Integrating mitophagy and ferroptosis in endometrial carcinogenesis (Review).Oncology letters · 2026Review
- Mechanism of LncRNA NORAD regulating ferroptosis in endometrial cancer cells by modifying GPX4 through FTO-mediated m6A methylation.Cellular and molecular life sciences : CMLS · 2025Article
- METTL5 regulates SEPHS2-mediated selenoprotein synthesis to promote multiple myeloma survival and progression.Cell death & disease · 2025Article
- Identification of clusters related to programmed cell death and potential prognostic biomarkers for immunotherapy response in endometrial cancer.Scientific reports · 2025Article
- Reprogrammed immuno-metabolic environment of cancer: the driving force of ferroptosis resistance.Molecular cancer · 2025Review
- SENP5 promotes endometrial cancer cell growth by regulating β-catenin deSUMOylation to enhance GPX4-resistance to ferroptosis.European journal of medical research · 2025Article
- Transferrin Receptor Promotes Endometrial Cancer Proliferation by Activating the Iron-Dependent PI3K/AKT/mTOR Signaling Pathway.Cancer science · 2025Article
- Exploring cell death pathways in oral cancer: mechanisms, therapeutic strategies, and future perspectives.Discover oncology · 2025Review
- Weight Management for Fertility-Preservation Therapy in Endometrial Cancer: Opportunities and Challenges.Current oncology reports · 2025Review
- Immune cell infiltration as a prognostic factor in endometrial cancer: a meta-analysis.American journal of cancer research · 2025Article
- Construction of a prognostic model for endometrial cancer related to programmed cell death using WGCNA and machine learning algorithms.Frontiers in immunology · 2025Article
- Establishment of a prognostic signature and immune infiltration characteristics for uterine corpus endometrial carcinoma based on a disulfidptosis/ferroptosis-associated signature.Frontiers in immunology · 2025Article
- Ferroptosis in the tumor microenvironment: mechanisms, advances, and therapeutic perspectives.Frontiers in oncology · 2025Review
- Harnessing the gut microbiome to modulate ferroptosis: a metabolic strategy for the treatment of digestive tract cancers.Frontiers in immunology · 2025Review
- Integrated Identification and Immunotherapy Response Analysis of the Prognostic Signature Associated With m6A, Cuproptosis-Related, Ferroptosis-Related lncRNA in Endometrial Cancer.Cancer reports (Hoboken, N.J.) · 2024Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Ferroptosis is a newly discovered form of regulated cell death. The main feature of ferroptosis is excessive membrane lipid peroxidation caused by iron-mediated chemical and enzymatic reactions. In normal cells, harmful lipid peroxides are neutralized by glutathione peroxidase 4 (GPX4). When GPX4 is inhibited, ferroptosis occurs. In mammalian cells, ferroptosis serves as a tumor suppression mechanism. Not surprisingly, in recent years, ferroptosis induction has gained attention as a potential anticancer strategy, alone or in combination with other conventional therapies. However, sensitivity to ferroptosis inducers depends on the metabolic state of the cell. Endometrial cancer (EC) is the sixth most common cancer in the world, with more than 66,000 new cases diagnosed every year. Out of all gynecological cancers, carcinogenesis of EC is mostly dependent on metabolic abnormalities. Changes in the uptake and catabolism of iron, lipids, glucose, and glutamine affect the redox capacity of EC cells and, consequently, their sensitivity to ferroptosis-inducing agents. In addition to this, in EC cells, ferroptosis-related genes are usually mutated and overexpressed, which makes ferroptosis a promising target for EC prediction, diagnosis, and therapy. However, for a successful application of ferroptosis, the connection between metabolic rewiring and ferroptosis in EC needs to be deciphered, which is the focus of this review.
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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.