ArticleOncogene2023
SLC35F2-SYVN1-TRIM59 axis critically regulates ferroptosis of pancreatic cancer cells by inhibiting endogenous p53.
Article in Oncogene, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- TRIM59 Drives Bladder Cancer Progression Through E3 Ligase-Dependent K48-Linked Degradation of PTRF.Cancer science · 2026Article
- Mechanisms and functions of the TRIM protein family in digestive system cancers.Journal of translational medicine · 2026Review
- The ubiquitin E3 ligase TRIM59 in myeloid cell regulates complement C3 through degrading CCAAT/enhancer binding protein β to promote neuron survival after ischemic stroke.Cell & bioscience · 2026Article
- Separating the genetics of disease, treatment, and treatment response using graphical modeling and large-scale electronic health records.medRxiv : the preprint server for health sciences · 2026Article
- TRIM59 alleviates neuronal ferroptosis and promotes functional recovery after spinal cord injury by mediating ubiquitination and degradation of ANXA2.Journal of orthopaedic translation · 2026Article
- Ferroptosis in cancer toward molecular insights and clinical translation in pancreatic cancer.Molecular cancer · 2026Review
- TRIM59 promotes immune evasion and tumor progression in lung adenocarcinoma via ubiquitin- proteasomal degradation of IRF3.Frontiers in immunology · 2026Article
- Post-Translational Modifications: Key "Regulators" of Pancreatic Cancer Malignant Phenotype-Advances in Mechanisms and Targeted Therapies.Biomedicines · 2025Review
- Sodium-myoinositol cotransporter-1 downstream of m6A methyltransferase WTAP exerts a potential carcinogenicity in diffuse large B-cell lymphoma progression.Journal of translational medicine · 2025Article
- Targeting the SYVN1-EGFR axis: a breakthrough strategy for TKI-resistant NSCLC.Cell death & disease · 2025Article
- Preliminary Exploration of the Osteogenic Differentiation Mechanism of Bone Marrow Mesenchymal Stem Cells Regulated by SYVN1.Journal of musculoskeletal & neuronal interactions · 2025Article
- TRIM59/RBPJ positive feedback circuit confers gemcitabine resistance in pancreatic cancer by activating the Notch signaling pathway.Cell death & disease · 2024Article
- Ferroptosis, a therapeutic target for cardiovascular diseases, neurodegenerative diseases and cancer.Journal of translational medicine · 2024Review
- IL15RA-STAT3-GPX4/ACSL3 signaling leads to ferroptosis resistance in pancreatic cancer.Acta biochimica et biophysica Sinica · 2024Article
- The Syvn1 inhibits neuronal cell ferroptosis by activating Stat3/Gpx4 axis in rat with spinal cord injury.Cell proliferation · 2024Article
- TRIM25, TRIM28 and TRIM59 and Their Protein Partners in Cancer Signaling Crosstalk: Potential Novel Therapeutic Targets for Cancer.Current issues in molecular biology · 2024Review
- Article
- Overexpression of SLC35F2 is a potential prognostic biomarker for lung adenocarcinoma.Heliyon · 2024Article
- Myeloid CellJournal of inflammation research · 2024Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer cells undergo intricate metabolic reprogramming to sustain their survival and proliferation. p53 exhibits a dual role in tumor cell ferroptosis. However, the precise role and mechanisms underlying wild-type p53 activation in promoting ferroptosis in pancreatic cancer cells remain obscure. In this study, we applied bioinformatics tools and performed an analysis of clinical tissue sample databases and observed a significantly upregulated expression of solute carrier family 35 member F2 (SLC35F2) in pancreatic cancer tissues. Our clinical investigations indicated that elevated SLC35F expression was related to adverse survival outcomes. Through multi-omics analyses, we discerned that SLC35F2 influences the transcriptome and inhibits ferroptosis in pancreatic cancer cells. Moreover, our findings reveal the pivotal involvement of p53 in mediating SLC35F2-mediated ferroptosis, both in vitro and in vivo. SLC35F2 inhibits ferroptosis by facilitating TRIM59-mediated p53 degradation. Further mechanistic investigations demonstrated that SLC35F2 competitively interacts with the E3 ubiquitin ligase SYVN1 of TRIM59, thereby stabilizing TRIM59 expression and consequentially promoting p53 degradation. Utilizing protein 3D structure analysis and drug screening, we identified irinotecan hydrochloride and lapatinib ditosylate as compounds targeting SLC35F2, augmenting the antitumor effect of imidazole ketone erastin (IKE) in a wild-type p53 patient-derived xenograft (PDX) model. However, in the p53 mutant PDX model, irinotecan hydrochloride and lapatinib ditosylate did not alter the sensitivity of the tumor xenograft model to IKE-triggered ferroptosis. In summary, our work establishes a novel mechanism wherein the SLC35F2-SYVN1-TRIM59 axis critically regulates ferroptosis of pancreatic cancer cells by inhibiting endogenous p53. Thus, SLC35F2 emerges as a promising therapeutic target for treating pancreatic cancer.
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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.