ArticleMolecular cancer2025
Cancer cells avoid ferroptosis induced by immune cells via fatty acid binding proteins.
Article in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed.
- Role of the circadian rhythm in squamous cell carcinoma: From molecular mechanism to therapy (Review).Molecular medicine reports · 2026Review
- Ferroptosis in cancer: molecular mechanisms, biological roles, and therapeutic significance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Sprayable hydrogel loaded with engineered fusion cellular vesicles for cancer recurrence suppression.Journal of nanobiotechnology · 2026Article
- LPCAT3 is essential for leukemia progression and represents a therapeutic vulnerability in AML.Blood science (Baltimore, Md.) · 2026Article
- Metabolic Reprogramming in Glioblastoma Stem Cells Promotes Radiation Resistance Through a H3K18la/USP30/MBOAT2 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cancer drug response and resistance: molecular mechanisms and combating strategies.Signal transduction and targeted therapy · 2026Review
- Mitochondrial Carrier SLC25A13 Drives Ferroptosis Resistance and Immune Evasion via a STAT3-IFI6 Circuit in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Rethinking LPCAT3 roles in human disease: broadening perspectives beyond ferroptosis.Cell death & disease · 2026Review
- The interplay between loneliness, cortisol, and NK cell function: The role of cortisol in NK cell dysfunction.Psychoneuroendocrinology · 2026Article
- CD8MedComm · 2026Review
- FABP7: A Regulator of Neuro-Immune Metabolic Networks and Therapeutic Vulnerabilities in Glioma.Cancers · 2026Review
- Integrating Radiomics and Computational Pathology to Predict Early Recurrence of Pancreatic Ductal Adenocarcinoma and Uncover Its Biological Basis in Tumor Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting YRDC blocks codon-biased FABP7 translation and lipid droplet formation to overcome chemoresistance in glioblastoma.Oncogene · 2026Article
- Multifunctional Role of Mitochondrial Fatty Acid Oxidation in Cancer Immunotherapy and Aging.Cancer science · 2026Review
- Regulated cell death programs shaping cancer therapy.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- EXOSC4 as a novel regulator of neddylation in acute myeloid leukemia.Scientific reports · 2026Article
- Lipid metabolism reprogramming shapes the immune landscape in the tumor microenvironment.Cellular & molecular immunology · 2026Review
- Review
- Article
- Multi-omics integration analysis reveals metabolic changes during sika deer antler growth.BMC genomics · 2026Article
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Authors and funding
30 authors.
Funding
Abstract
backgroundCancer creates an immunosuppressive environment that hampers immune responses, allowing tumors to grow and resist therapy. One way the immune system fights back is by inducing ferroptosis, a type of cell death, in tumor cells through CD8
methodsTo explore how cancer cells resist immune cell-mediated ferroptosis, we used a comprehensive range of techniques. We worked with cell lines including PD1-sensitive, PD1-resistant, B16F10, and QPP7 glioblastoma cells, and conducted in vivo studies in syngeneic 129 Sv/Ev, C57BL/6, and conditional knockout mice with Rora deletion specifically in CD8
resultsPD1-resistant tumors upregulate Fabp7, driving protective metabolic changes that shield cells from ferroptosis and evade anti-tumor immunity. Fabp7 decreases the transcription of ferroptosis-inducing genes like Lpcat3 and increases the transcription of ferroptosis-protective genes such as Bmal1 through epigenetic reprogramming. Lipidomic profiling revealed that Fabp7 increases triglycerides and monounsaturated fatty acids (MUFAs), which impede lipid peroxidation and ROS generation. Fabp7 also improves mitochondrial function and fatty acid oxidation (FAO), enhancing cancer cell survival. Furthermore, cancer cells increase Fabp7 expression in CD8
conclusionsOur study uncovers a novel mechanism by which cancer cells evade immune-mediated ferroptosis through Fabp7 upregulation. This protein reprograms lipid metabolism and disrupts circadian regulation in immune cells, promoting tumor survival and resistance to immunotherapy. Targeting Fabp7 could enhance immunotherapy effectiveness by re-sensitizing resistant tumors to ferroptosis.
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