ArticleBMC cancer2022
GPX4 suppresses ferroptosis to promote malignant progression of endometrial carcinoma via transcriptional activation by ELK1.
Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- CL-316243 facilitates stable atherosclerotic plaque phenotypes in association with suppression of perivascular adipose tissue ferroptosis via upregulating C/EBPβ.Redox biology · 2026Article
- Mitochondria as integrative regulators of ferroptosis in the female reproductive system.Biology of reproduction · 2026Review
- Uncovering the mechanism of DCLK3 in colorectal cancer progression through WGCNA and machine learning.BMC cancer · 2026Article
- The crosslink between autophagy and ferroptosis in polycystic ovary syndrome: from synergistic pathogenesis to targeted therapy.Journal of ovarian research · 2026Review
- LINC00839 transcriptionally activated by ELK1 represses ferroptosis in nasopharyngeal carcinoma by regulating UPF1/RCHY1/DJ-1 axis.NPJ precision oncology · 2026Article
- Ferroptosis as a novel targeted therapy in gynecological malignant tumors.Discover oncology · 2026Review
- Inducing Ferroptosis: Sensitization Strategy for Radiotherapy and Its Application.Antioxidants (Basel, Switzerland) · 2026Review
- Ferroptosis and Alzheimer's disease: a new insight into neurodegeneration.Frontiers in immunology · 2026Review
- Interplay of oxidative stress and antioxidant mechanisms in cancer development and progression.Archives of toxicology · 2026Review
- Oxidative stress as a nexus: Integrating mitophagy and ferroptosis in endometrial carcinogenesis (Review).Oncology letters · 2026Review
- Biallelic BRF2 mutations disrupt redox homeostasis as etiological factors in syndromic immunodeficiency and developmental disorders.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- 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
- Mitochondrial HSP90 Paralog TRAP1 Deletion Drives Glutamine Addiction in Tumor Cells via Destablization of the Cys/Glu Antiporter SLC7A11/xCT.Molecular cancer research : MCR · 2025Article
- Mechanistic Insights and Clinical Implications of ELK1 in Solid Tumors: A Narrative Review.Cells · 2025Review
- 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
- T-Box Transcription Factor 2 Mediates Chemoresistance of Endometrial Cancer via Regulating FSP1-involved Ferroptosis.Cell biochemistry and biophysics · 2025Article
- ETS-1 in tumor immunology: implications for novel anti-cancer strategies.Frontiers in immunology · 2025Review
- KLF14 directly downregulates the expression of GPX4 to exert antitumor effects by promoting ferroptosis in cervical cancer.Journal of translational medicine · 2024Article
- Role of ferroptosis in radiation-induced soft tissue injury.Cell death discovery · 2024Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlutathione Peroxidase 4 (GPX4) is a key protein that inhibits ferroptosis. However, its biological regulation and mechanism in endometrial cancer (EC) have not been reported in detail.
methodsThe expression of GPX4 in EC tissues was determined by TCGA databases, qRT-PCR, Western blot, and immunohistochemistry (IHC). The effects of GPX4 on EC cell proliferation, migration, apoptosis, and tumorigenesis were studied in vivo and in vitro. In addition, ETS Transcription Factor ELK1 (ELK1) was identified by bioinformatics methods, dual-luciferase reporter assay, and chromatin immunoprecipitation (ChIP). Pearson correlation analysis was used to evaluate the association between ELK1 and GPX4 expression.
resultsThe expression of GPX4 was significantly up-regulated in EC tissues and cell lines. Silencing GPX4 significantly inhibited the proliferation, migration ability, induced apoptosis, and arrested the cell cycle of Ishikawa and KLE cells. Knockdown of GPX4 accumulated intracellular ferrous iron and ROS, disrupted MMP, and increased MDA levels. The xenograft tumor model also showed that GPX4 knockdown markedly reduced tumor growth in mice. Mechanically, ELK1 could bind to the promoter of GPX4 to promote its transcription. In addition, the expression of ELK1 in EC was positively correlated with GPX4. Rescue experiments confirmed that GPX4 knockdown could reverse the strengthens of cell proliferation and migration ability and the lower level of Fe
conclusionThe results of the present study suggest that ELK1 / GPX4 axis plays an important role in the progress of EC by promoting the malignant biological behavior and inducing ferroptosis of EC cells, which provides evidence for investigating the potential therapeutic strategies of endometrial cancer.
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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.