ArticleMolecular cancer2022
N
Article in Molecular cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 69 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- The relationship between the network of non-coding RNAs-molecular targets and N6-methyladenosine modification in tumors of urinary system.Cell death & disease · 2024Pooled it
- CircLAMA5 traps Sam68 in the cytoplasm to regulate alternative splicing and drive sunitinib resistance in ccRCC.Oncogene · 2026Article
- N6-Methyladenosine RNA Methylation: A Key Regulator in Male Reproductive Disorders and Urological Cancers.The world journal of men's health · 2026Review
- WTAP-mediated mMolecular genetics and genomics : MGG · 2026Article
- RNA methylation in cell death: mechanisms and clinical applications.Molecular cancer · 2026Review
- Methyltransferase-Like 14 Promotes the Angiogenesis of Hepatocellular Carcinoma via Targeting Vascular Endothelial Growth Factor A.Cancer reports (Hoboken, N.J.) · 2026Article
- The crucial role of m6A methylation modification in nasopharyngeal carcinoma.Discover oncology · 2026Review
- The identification of genes related to METTL14 inhibition in radiation-induced hepatocyte death based on bioinformatics analysis.Scientific reports · 2026Article
- METTL14-Mediated Inhibition of Apoptosis via the MAPK and PI3K/AKT Pathways PromotesMicroorganisms · 2026Article
- Unveiling the epigenetic landscape: transforming renal cell carcinoma treatment.Clinical epigenetics · 2026Review
- PDZK1-ULK1 Axis Triggers Lipophagy to Inhibit Tumor Progression and Sunitinib Resistance in Clear Cell Renal Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Correction: N6‑methyladenosine‑modified TRAF1 promotes sunitinib resistance by regulating apoptosis and angiogenesis in a METTL14‑dependent manner in renal cell carcinoma.Molecular cancer · 2026Article
- Differences in the expression profiles of m6A-related genes and the prognostic role in immunotherapy for lung adenocarcinoma patients.Frontiers in oncology · 2026Article
- The dual regulatory role of METTL14-mediated mFrontiers in oncology · 2026Review
- ALYREF-mediated mInternational journal of biological sciences · 2026Article
- PRMT3 in cancer: arginine methylation as a driver of tumor metabolism, immune evasion, and therapeutic resistance.Frontiers in immunology · 2026Review
- Influence of RNA Modifications on Cancer Metabolism: Interplay with Hypoxia and Therapeutic Implications.Advances in experimental medicine and biology · 2026Review
- Dapagliflozin alleviates sunitinib-induced cardiotoxicity through AMPKα-PPARα axis and enhances the sensitivity of renal cell carcinoma to sunitinib.BMC medicine · 2025Article
- ERβ/circAHNAK Axis Inhibits USP10-FMR1 Deubiquitination to Prevent m⁶A-Mediated ADAM17 Decay and Promote Angiogenesis in Clear Cell Renal Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- METTL14 Regulates the Expression of Genes Related to Interferon, Interleukin and MHC Class I in Nasopharyngeal Carcinoma Cells.Cancer medicine · 2025Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSunitinib resistance can be classified into primary and secondary resistance. While accumulating research has indicated several underlying factors contributing to sunitinib resistance, the precise mechanisms in renal cell carcinoma are still unclear.
methodsRNA sequencing and m6A sequencing were used to screen for functional genes involved in sunitinib resistance. In vitro and in vivo experiments were carried out and patient samples and clinical information were obtained for clinical analysis.
resultsWe identified a tumor necrosis factor receptor-associated factor, TRAF1, that was significantly increased in sunitinib-resistant cells, resistant cell-derived xenograft (CDX-R) models and clinical patients with sunitinib resistance. Silencing TRAF1 increased sunitinib-induced apoptotic and antiangiogenic effects. Mechanistically, the upregulated level of TRAF1 in sunitinib-resistant cells was derived from increased TRAF1 RNA stability, which was caused by an increased level of N6-methyladenosine (m6A) in a METTL14-dependent manner. Moreover, in vivo adeno-associated virus 9 (AAV9) -mediated transduction of TRAF1 suppressed the sunitinib-induced apoptotic and antiangiogenic effects in the CDX models, whereas knockdown of TRAF1 effectively resensitized the sunitinib-resistant CDXs to sunitinib treatment.
conclusionsOverexpression of TRAF1 promotes sunitinib resistance by modulating apoptotic and angiogenic pathways in a METTL14-dependent manner. Targeting TRAF1 and its pathways may be a novel pharmaceutical intervention for sunitinib-treated patients.
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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.