ArticleCell death & disease2025
Dimethyl fumarate promotes the degradation of HNF1B and suppresses the progression of clear cell renal cell carcinoma.
Article in Cell death & disease, 2025. 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 9 papers.
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Who cites it
9 citing papers in PubMed.
- A Pan-Cancer Single-Cell Atlas to Evaluate Tumor Identity, Cell Line Concordance, and Dependency Mapping.bioRxiv : the preprint server for biology · 2026Article
- Programmed cell death inhibitors: a new hope for cancer therapy?World journal of surgical oncology · 2026Review
- GFPT2 drives sunitinib resistance of renal cell carcinoma via enzyme-dependent and -independent manners.International journal of biological sciences · 2026Article
- Dual targeting of the UPS and autophagy as a novel therapy for neurodegenerative proteinopathies.Frontiers in cellular neuroscience · 2026Review
- Functional regulatory roles of HNF1B in promoting cell proliferation, migration, invasion and fate decision of hepatocellular carcinoma.BMC cancer · 2025Article
- Dimethyl Fumarate vs. Monomethyl Fumarate: Unresolved Pharmacologic Issues.Pharmaceutics · 2025Review
- Local photocrosslinking of native tissue matrix regulates lung epithelial cell mechanosensing and function.Nature materials · 2025Article
- An Experimental Rat Model for Simultaneous Induction of Peripheral Neuropathy and Myelotoxicity by Docetaxel Administration: Evaluating the Protective Role of Dimethyl Fumarate.International journal of molecular sciences · 2025Article
- Repurposing dimethyl fumarate for cancer therapy: current evidence and future directions.Frontiers in pharmacology · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
15 authors.
Funding
Abstract
Clear cell renal cell carcinoma (ccRCC) is the most lethal subtype of renal cancer, and its treatment options remain limited. Therefore, there is an urgent need to discover therapeutic agents for ccRCC treatment. Here, we demonstrate that dimethyl fumarate (DMF), an approved medication for multiple sclerosis [1] and psoriasis, can inhibit the proliferation of ccRCC cells. Mechanistically, hepatocyte nuclear factor 1β (HNF1B), a transcription factor highly expressed in ccRCC, is succinated by DMF at cysteine residues, leading to its proteasomal degradation. Furthermore, HNF1B interacts with and stabilizes Yes-associated protein (YAP), thus DMF-mediated HNF1B degradation decreases YAP protein level and the expression of its target genes, resulting in the suppression of ccRCC cell proliferation. Importantly, oral administration of DMF sensitizes ccRCC to sunitinib treatment and enhances its efficacy in mice. In summary, we provide evidences supporting DMF as a potential drug for clinical treatment of ccRCC by targeting HNF1B and reveal a previously unrecognized role of HNF1B in regulating YAP in ccRCC.
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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.