ArticleNature communications2025
S100P is a ferroptosis suppressor to facilitate hepatocellular carcinoma development by rewiring lipid metabolism.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Ferroptosis in liver biology and diseases.Hepatology communications · 2026Review
- Identifying JAK2 and ANXA5 as Key Genes Linking Obstructive Sleep Apnea and Oxidative Stress via Machine Learning and Multilayer Transcriptomic Integration With Functional Validation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Dual Compartmentalization of GSTA4 Suppresses Ferroptosis to Drive Antiandrogen Resistance in Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ferroptosis: Newly Emerged Regulator for Human Disease.MedComm · 2026Review
- Post-translational modifications in metabolic reprogramming: implications for metabolic therapy and immunotherapy in cancer.Signal transduction and targeted therapy · 2026Review
- Piezoelectric Nanozymes With Acoustically Rejuvenated Catalytic Activities Rewire Lipid Metabolism for Two-Pronged Ferroptotic Therapy.Angewandte Chemie (International ed. in English) · 2026Article
- Article
- Fatty acid synthesis therapy-induced senescence (FASTIS) in cancer cells.Cell death & disease · 2026Article
- Deciphering Lipid Metabolic Landscape of Sorafenib-Treated Hepatocellular Carcinoma by Mass Spectrometry Imaging and Transcriptomics.Biomolecules · 2026Article
- Fatty acid metabolic reprogramming in the tumor microenvironment: Unraveling mechanisms and therapeutic prospects.Genes & diseases · 2026Review
- S100P mediates IL-13/ATF4-driven epithelial barrier dysfunction in eosinophilic asthma: a potential biomarker and therapeutic target.Journal of translational medicine · 2026Article
- Targeting Wnt3a and Loxl2 Synergistically Induces Ferroptosis in Liver Cancer Stem Cells and Suppresses Tumorigenesis.Cancer science · 2026Article
- Single-cell transcriptomic mapping of patient-derived primary liver cancer organoids reveals molecular subtypes and guides precision drug targeting.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- The controversial role of metabolic reprogramming in anti-tumor therapy resistance.Discover oncology · 2026Review
- Ferroptosis-autophagy crosstalk in bladder cancer: mechanisms and therapeutic implications.Molecular cancer · 2026Review
- Multi-omics analysis reveals that CAPG positive macrophages are key immunosuppressive drivers and prognostic determinants in the ferroptosis landscape of hepatocellular carcinoma.Discover oncology · 2026Article
- A prognostic signature of ferroptosis and lipid metabolism related genes predicts survival and immunotherapy response in hepatocellular carcinoma.Discover oncology · 2026Article
- Mechanistic insights into ferroptosis and its therapeutic potential in hepatocellular carcinoma.Frontiers in immunology · 2026Review
- The Role of Mitochondrial Dysfunction in Hepatocellular Carcinoma: From Pathogenesis and Drug Resistance to Targeted Therapeutic Strategies.Journal of hepatocellular carcinoma · 2026Review
- Bimodal regulation and precision therapy of neutrophil extracellular traps in liver ischemia-reperfusion injury: recent advances.Frontiers in immunology · 2026Review
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Authors and funding
11 authors.
Funding
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Abstract
Ferroptosis is a newly identified programmed cell death induced by iron-driven lipid peroxidation and implicated as a potential approach for tumor treatment. However, emerging evidence indicates that hepatocellular carcinoma (HCC) cells are generally resistant to ferroptosis and the underlying molecular mechanism is poorly understood. Here, our study confirms that S100 calcium binding protein P (S100P), which is significantly up-regulated in ferroptosis-resistant HCC cells, efficiently inhibits ferroptosis. Mechanistically, S100P facilitates lysosomal degradation of acetyl-CoA carboxylase alpha (ACC1), which is indispensable for de novo biosynthesis of lipids. Loss of S100P elevates the expression of ACC1 and promotes ferroptotic sensitivity of HCC cells. S100P-mediated ACC1 degradation relies on RAB5C, which directs ACC1 to lysosome via P62-dependent selective autophagy. Knockdown of RAB5C or P62 abrogates S100P-induced lysosomal degradation of ACC1 and restores resistance of HCC cells to ferroptosis. Our work reveals an alternative anti-ferroptosis pathway and suggests S100P as a promising druggable target for ferroptosis-related therapy of HCC.
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