ArticleCell death & disease2024
USP43 stabilizes c-Myc to promote glycolysis and metastasis in bladder cancer.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 56 citations in OpenAlex.
- Triptolide as a multi-target anticancer agent: molecular mechanisms and translational potential.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- LncRMRP drives bladder cancer invasion via a lactylation-driven positive feedback circuit.Oncogene · 2026Article
- Lactate metabolism and protein lactylation in inflammatory and tumor microenvironments.Molecular biomedicine · 2026Review
- Lethal clinical outcome and immuno-fibrotic contexture in refractory urothelial carcinoma harboring MYC amplification and overexpression.British journal of cancer · 2026Article
- MYC in Oncogenesis and Therapeutic Implications.MedComm · 2026Review
- USP43-mediated deubiquitination of SLC7A11 protects against LPS-induced acute lung injury by inhibiting ferroptosis.Clinical and translational medicine · 2026Article
- DNMT1 methylates E3 ligase FBXO32 to regulate Myc stability and glycolytic reprogramming in diabetic retinopathy associated endothelial cells.Journal of bioenergetics and biomembranes · 2026Article
- Identification of MYC co-expression gene: POLR3G is associated with cell senescence, immunotherapy, chemotherapy responses, and clinical prognosis in bladder cancer patients.Translational oncology · 2026Article
- Oncogene c‑Myc: From molecular mechanism to targeted therapy (Review).Molecular medicine reports · 2026Review
- Deubiquitinase USP43 exacerbates myocardial ischemia-reperfusion injury by stabilizing ASK1 and activating the JNK/P38 MAPK pathway.Basic research in cardiology · 2026Article
- Nucleic Acid Therapeutics for "Undruggable" Cancer Targets: Mechanisms, Challenges, and Prospects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- H3K18 lactylation promotes glycolysis in bladder cancer via inhibiting GNG7 through regulating PI3K-AKT signaling pathway.World journal of surgical oncology · 2026Article
- USP43 Inhibits Intestinal Inflammation via TRAF4-mediated NF-κB Signaling.Inflammation · 2026Article
- USP5 in cancer: a therapeutic window into metabolism and drug resistance.Journal of translational medicine · 2026Review
- FBXL6 promotes bladder cancer progression by stabilizing ENO1 through K63-linked ubiquitination.Cell death discovery · 2026Article
- Nuclear hexokinase 2 couples hyperglycemia to MYC-driven glycolytic and stemness programs in bladder cancer.Cell death & disease · 2026Article
- Inhibition of ZBTB7B-mediated ADPGK transcription by NEDD4 impedes glycolysis and progression of lung adenocarcinoma.Oncogenesis · 2026Article
- Targeting Glycolytic Metabolism in Cancer Therapy: Current Approaches and Future Perspectives.Cells · 2026Review
- HDAC5 deficiency induces intrinsic resistance to KRAS inhibition by disrupting c-Myc acetylation-ubiquitination homeostasis.The Journal of clinical investigation · 2026Article
- YKT6 Promotes Bladder Cancer Progression by Stabilizing β-catenin Through USP7-Mediated Deubiquitination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A hallmark of tumor cells, including bladder cancer (BLCA) cells, is metabolic reprogramming toward aerobic glycolysis (Warburg effect). The classical oncogene MYC, which is crucial in regulating glycolysis, is amplified and activated in BLCA. However, direct targeting of the c-Myc oncoprotein, which regulates glycolytic metabolism, presents great challenges and necessitates the discovery of a more clarified regulatory mechanism to develop selective targeted therapy. In this study, a siRNA library targeting deubiquitinases identified a candidate enzyme named USP43, which may regulate glycolytic metabolism and c-Myc transcriptional activity. Further investigation using functional assays and molecular studies revealed a USP43/c-Myc positive feedback loop that contributes to the progression of BLCA. Moreover, USP43 stabilizes c-Myc by deubiquitinating c-Myc at K148 and K289 primarily through deubiquitinase activity. Additionally, upregulation of USP43 protein in BLCA increased the chance of interaction with c-Myc and interfered with FBXW7 access and degradation of c-Myc. These findings suggest that USP43 is a potential therapeutic target for indirectly targeting glycolytic metabolism and the c-Myc oncoprotein consequently enhancing the efficacy of bladder cancer treatment.
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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.