ArticleCell death discovery2025
SREBF1-based metabolic reprogramming in prostate cancer promotes tumor ferroptosis resistance.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Ferroptosis research based on bibliometric and visual analysis: mechanism exploration and clinical application prospects in gastric cancer, prostate cancer, leukemia, and brain tumors.Frontiers in medicine · 2025Pooled it
- Metabolic reprogramming in colorectal cancer: Mechanisms and therapeutic insights.Genes & diseases · 2027Review
- Targeting ACSF2 overcomes Ara-C resistance in acute myeloid leukemia via the cholesterol metabolism-ERK signaling axis.Leukemia · 2026Article
- Sterol regulatory element‑binding proteins: Master regulators of lipid metabolic reprogramming in cancer and emerging therapeutic targets (Review).Oncology reports · 2026Review
- ERBB2 as a Prognostic Biomarker in Prostate Cancer: Integration of Single-Cell Transcriptomics, Deep Learning, and Immunohistochemical Validation.Biochemical genetics · 2026Article
- A fatty acid metabolism-based deep learning model predicts biochemical recurrence and identifies NUDT19 as a candidate metabolic factor in prostate cancer.World journal of surgical oncology · 2026Article
- A Review ofFoods (Basel, Switzerland) · 2026Review
- Deep learning for predicting pituitary neuroendocrine tumour lineage and high-risk subtypes from histology.NPJ precision oncology · 2026Article
- SREBP1-activated lipid metabolism drives ferroptosis and progression of clear cell renal cell carcinoma.Science China. Life sciences · 2026Article
- Construction of a survival model for predicting biochemical recurrence of prostate cancer based on propionate metabolism-related genes.Translational andrology and urology · 2026Article
- Metabolic reprogramming in cancer: dysregulation of glucose, lipid, and amino acid pathways and therapeutic opportunities.Molecular biomedicine · 2026Review
- SOX8/CPT2 axis regulates lipid metabolism to support enzalutamide resistance in prostate cancer.Cancer cell international · 2026Article
- Metabolic-Immune Coupling in Urologic Cancers: Macrophage Reprogramming as a Therapeutic Nexus.International journal of biological sciences · 2026Review
- Multi-omics genetic study revealing ferroptosis regulator CTSB driving prostate cancer progression by modulating the immune microenvironment.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Tumor microenvironment-mediated immune evasion and resistance in prostate cancer: mechanisms, cross-talk, and therapeutic opportunities.Clinical and experimental medicine · 2025Review
- Circulating chromatin reveals the effects of disease-associated variants on gene regulation.bioRxiv : the preprint server for biology · 2025Article
- Reprogrammed Lipid Metabolism-Associated Therapeutic Vulnerabilities in Prostate Cancer.International journal of molecular sciences · 2025Review
- Unraveling SREBF1's role in elevating colorectal cancer prognosis through proliferation and migration inhibition.PloS one · 2025Article
- Mitochondrial involvement in PC: improving therapeutic strategies.Frontiers in pharmacology · 2025Review
- The role of neuroendocrine differentiation in treatment resistance of prostate cancer and intervention strategies.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic reprogramming in prostate cancer has been widely recognized as a promoter of tumor progression and treatment resistance. This study investigated its association with ferroptosis resistance in prostate cancer and explored its therapeutic potential. In this study, we identified differences in the epithelial characteristics between normal prostate tissue and tissues of various types of prostate cancer using single-cell sequencing. Through transcription factor regulatory network analysis, we focused on the candidate transcription factor, SREBF1. We identified the differences in SREBF1 transcriptional activity and its association with ferroptosis, and further verified this association using hdWGCNA. We constructed a risk score based on SREBF1 target genes associated with the biochemical recurrence of prostate cancer by combining bulk RNA analysis. Finally, we verified the effects of the SREBPs inhibitor Betulin on the treatment of prostate cancer and its chemosensitization effect. We observed characteristic differences in fatty acid and cholesterol metabolism between normal prostate tissue and prostate cancer tissue, identifying high transcriptional activity of SREBF1 in prostate cancer tissue. This indicates that SREBF1 is crucial for the metabolic reprogramming of prostate cancer, and that its mediated metabolic changes promoted ferroptosis resistance in prostate cancer in multiple ways. SREBF1 target genes are associated with biochemical recurrence of prostate cancer. Finally, our experiments verified that SREBF1 inhibitors can significantly promote an increase in ROS, the decrease in GSH, and the decrease in mitochondrial membrane potential in prostate cancer cells and confirmed their chemosensitization effect in vivo. Our findings highlighted a close association between SREBF1 and ferroptosis resistance in prostate cancer. SREBF1 significantly influences metabolic reprogramming in prostate cancer cells, leading to ferroptosis resistance. Importantly, our results demonstrated that SREBF1 inhibitors can significantly enhance the therapeutic effect and chemosensitization of prostate cancer, suggesting a promising therapeutic potential for the treatment of prostate cancer.
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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 OpenQuestion graph.