ArticleApoptosis : an international journal on programmed cell death2026
SREBP2 confers ferroptosis resistance by targeting GPX4 in colorectal cancer.
Article in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- SREBF2 promotes mitophagy and protects against ferroptosis via Cav-1-regulated PINK1/Parkin signaling in ischemic heart failure.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Sterol regulatory element‑binding proteins: Master regulators of lipid metabolic reprogramming in cancer and emerging therapeutic targets (Review).Oncology reports · 2026Review
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Authors and funding
13 authors.
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Abstract
backgroundThe upregulated expression of sterol regulatory element-binding protein 2 (SREBP2) has been observed in multiple types of malignant cancers. Ferroptosis is a form of cell death that is iron-dependent and driven by the accumulation of lipid peroxides. It has recently garnered considerable attention in Colorectal cancer (CRC) research. This study aims to investigate the role of SREBP2 in CRC ferroptosis resistance and the underlying molecular mechanisms.
methodsSREBP2 expression was assessed in CRC. Functional assays were conducted in HT29 and RKO cells following SREBP2 knockdown or treatment with Betulin, the SREBP2 inhibitor. RNA-seq was used to screen the potential downstream targets of SREBP2. Mechanistically, ferroptosis-related markers and rescue assays revealed the relation between SREBP2 and CRC ferroptosis resistance mediated by GPX4 expression regulation. Furthermore, ChIP and luciferase assays were used to confirm the upstream that regulates SREBP2 expression. Finally, subcutaneous tumorigenesis model was employed to evaluate the therapeutic potential of targeting SREBP2 in CRC.
resultsThe upregulated SREBP2 expression in CRC drives the proliferation, migration, and invasion of CRC cells. Mechanistically, SREBP2 directly increases GPX4 transcription, thereby reducing the sensitivity of CRC to ferroptosis and facilitating CRC progression. Additionally, β-catenin was identified as an upstream regulator of SREBP2. Inhibition of SREBP2 sensitizes CRC cells to ferroptosis and suppresses tumor growth.
conclusionSREBP2 enhances ferroptosis resistance in CRC by upregulating GPX4, thereby contributing to tumor progression. Our findings highlight SREBP2 as a potential therapeutic target and provide a rationale for the development of SREBP2-targeted strategies in colorectal cancer.
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