ArticleRedox biology2024
Excessive SOX8 reprograms energy and iron metabolism to prime hepatocellular carcinoma for ferroptosis.
Article in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 23 citations in OpenAlex.
- NOX2/NOX4-associated oxidative stress contributes to G6PD-associated metabolic remodeling and ferroptosis during mice luteolysis.Redox report : communications in free radical research · 2026Article
- SUV39H2-mediated NCOA4 methylation controls ferritinophagy and ferroptosis in triple-negative breast cancer.Cell death & disease · 2026Article
- SOX8/CPT2 axis regulates lipid metabolism to support enzalutamide resistance in prostate cancer.Cancer cell international · 2026Article
- Expression of lipid metabolism-related genes in hepatocellular carcinoma and their prognostic significance.Pakistan journal of medical sciences · 2026Article
- Mitochondrial LINC00942 activates complex I and inhibits ferroptosis through interacting with GRSF1 in liver cancer.Science China. Life sciences · 2026Article
- Post-Translational Modification Networks in Ferroptosis: Orchestrating Defense, Drug Resistance, and Therapeutic Opportunities in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2026Review
- Hyperoside promotes osteoblast differentiation by increasing osteoclast-derived migrasomes to alleviate osteoporosis.American journal of translational research · 2026Article
- Nucleophosmin 1 lactylation in graft kidney induces ferroptotic trigger waves that exacerbate delayed graft function.Nature communications · 2025Article
- Artesunate induces ferroptosis in gastric cancer by targeting the TFRC-HSPA9 axis for iron homeostasis regulation.Redox biology · 2025Article
- Ferritinophagy in cardiovascular diseases: mechanisms and potential therapy.Molecular and cellular biochemistry · 2025Review
- Targeting mitochondrial dysfunction to intervene in liver cancer.Cancer biology & medicine · 2025Review
- Article
- Role of the transcription factorTranslational cancer research · 2025Article
- Epigenetic crossroads in metabolic and cardiovascular health: the role of DNA methylation in type 2 diabetes and cardiovascular diseases.Cardiovascular diabetology · 2025Review
- Boric Acid Suppresses Glioblastoma Cellular Survival by Regulating Ferroptosis via SOX10/GPx4/ACSL4 Signalling and Iron Metabolism.Journal of cellular and molecular medicine · 2025Article
- Mitochondrial alterations and signatures in hepatocellular carcinoma.Cancer metastasis reviews · 2025Review
- Sox8: a multifaceted transcription factor in development and disease.Biology open · 2025Review
- Mitochondrial proteins: Potential pathophysiological mechanisms of malignant progression in HCC.PloS one · 2025Article
- Ferroptosis in ischemia-reperfusion injury: molecular mechanisms and therapeutic strategies.American journal of cardiovascular disease · 2025Review
- HDAC7 drives glioblastoma to a mesenchymal-like state via LGALS3-mediated crosstalk between cancer cells and macrophages.Theranostics · 2024Article
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipid peroxidation and redox imbalance are hallmarks of ferroptosis, an iron-dependent form of cell death. Growing evidence suggests that dysregulation in glycolipid metabolism and iron homeostasis substantially contribute to the development of hepatocellular carcinoma (HCC). However, there is still a lack of comprehensive understanding regarding the specific transcription factors that are capable of coordinating glycolipid and redox homeostasis to initiate the onset of ferroptosis. We discovered that overexpression of SOX8 leads to impaired mitochondria integrate, increased oxidative stress, and enhanced lipid peroxidation. These effects can be attributed to the inhibitory impact of SOX8 on de novo lipogenesis, glycolysis, the tricarboxylic acid cycle (TCA), and the pentose phosphate pathway (PPP). Additionally, upregulation of SOX8 results in reduced synthesis of NADPH, disturbance of redox homeostasis, disruption of mitochondrial structure, and impairment of the electron transport chain. Furthermore, the overexpression of SOX8 enhances the process of ferroptosis by upregulating the expression of genes associated with ferroptosis and elevating intracellular levels of ferrous ion. Importantly, the overexpressing of SOX8 has been observed to inhibit the proliferation of HCC in immunodeficient animal models. In conclusion, the findings suggest that SOX8 has the ability to alter glycolipid and iron metabolism of HCC cells, hence triggering the process of ferroptosis. The results of our study present a novel strategy for targeting ferroptosis in the therapy of HCC.
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