ArticleCell death discovery2026
SREBP1 knockdown triggers ferroptosis by suppressing the Nrf2-XCT/GPX4 axis in ovarian cancer.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
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Who cites it
4 citing papers in PubMed.
- Ferroptosis bridges early-life oxidative stress and lifetime meat quality defects in broilers.Poultry science · 2026Article
- The Impact of Oxidative Stress Imbalance on Ovarian Function and Its Mechanisms.International journal of general medicine · 2026Review
- Advances in ferroptosis research in ovarian cancer: molecular mechanisms and therapeutic perspectives.American journal of cancer research · 2026Review
- Natural products targeting the Nrf2 signaling pathway: potential targets and intervention strategies for the prevention and treatment of colorectal cancer.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Reprogramming of lipid metabolism is a hallmark of malignant tumors, and targeting key enzymes in lipid metabolism has emerged as a critical strategy to inhibit tumor progression. Sterol regulatory element-binding protein 1 (SREBP1), a master regulator of lipid biosynthesis, drives lipid metabolic reprogramming that not only promotes malignant progression but also confers resistance to ferroptosis in tumor cells. Ferroptosis is a distinct form of regulated cell death characterized by iron accumulation and lipid peroxidation. In this study, we demonstrate that silencing SREBP1 in ovarian cancer cells leads to decreased glutathione (GSH) levels, reduced protein expression of XCT and GPX4, and increased levels of malondialdehyde (MDA) and lipid peroxidation, indicating that SREBP1 silencing induces ferroptosis in ovarian cancer cells. Further experiments, including the CCK-8, EdU, colony formation assays and flow cytometry, confirmed that SREBP1 silencing suppresses proliferation by inducing cell cycle arrest. Transwell assays, immunofluorescence (IF) staining, Nile Rad staining, and measurements of triglyceride (TG) and total cholesterol (TC) levels demonstrated that SREBP1 silencing inhibits epithelial-mesenchymal transition (EMT) and lipid synthesis in ovarian cancer cells. Notably, SREBP1 silencing downregulates the expression of Nrf2, and treatment with the Nrf2 activator THBQ reverses the effects of SREBP1 silencing on ovarian cancer cell proliferation and ferroptosis. Mechanistically, SREBP1 silencing promotes ubiquitination-mediated degradation of the Nrf2 protein, thereby suppressing the expression of XCT and GPX4, ultimately triggering ferroptosis in ovarian cancer cells. Our findings establish SREBP1 as a key mediator of ferroptosis resistance and nominates it as both a therapeutic target and a potential prognostic biomarker in ovarian cancer. Schematic diagram illustrating the mechanism whereby silent SREBP1 mediates the Nrf2/XCT/GPX4 pathway to induce ferroptosis in ovarian cancer cells.
Identifiers
What Socratic holds
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 Socratic graph.