ArticleCancer science2021
The Warburg effect as a therapeutic target for bladder cancers and intratumoral heterogeneity in associated molecular targets.
Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 83 citations in OpenAlex.
- Intersection of Precision Nutrition and Bladder Cancer: A Narrative State-of-the-Art Review of Potential Applications and Challenges.Journal of clinical medicine · 2026Review
- Lactate Metabolism and Protein Lactylation in Diabetic Kidney Disease: A Narrative Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Glycolysis-mediated H3K18la modifications drive aggressive bladder cancer through metabolic and epigenetic reprogramming.Frontiers in immunology · 2026Article
- Aerobic glycolysis in bladder cancer: research advances and targeted therapy potential.Frontiers in oncology · 2026Review
- The interplay of dietary sugar, chronic inflammation, and bladder cancer: mechanistic insights, evidence, and prevention strategies.Frontiers in immunology · 2026Review
- Regulation of drug resistance in bladder urothelial carcinoma by tumor aerobic glycolysis.Journal of translational medicine · 2025Review
- Article
- Knockdown of LINC00467 inhibits gastric cancer progression by modulating the sequestration of miR-141-3p.Oncology letters · 2025Article
- CDCA3-MYC positive feedback loop promotes bladder cancer progression via ENO1-mediated glycolysis.Journal of experimental & clinical cancer research : CR · 2025Article
- Epigenetic dysregulation-induced metabolic reprogramming fuels tumor progression in bladder cancer.Frontiers in molecular biosciences · 2025Article
- Phenomics Demonstrates Cytokines Additive Induction of Epithelial to Mesenchymal Transition.Journal of cellular physiology · 2025Article
- ING5 inhibits aerobic glycolysis of lung cancer cells by promoting TIE1-mediated phosphorylation of pyruvate dehydrogenase kinase 1 at Y163.Frontiers of medicine · 2024Article
- Review
- Cisplatin-Resistant Urothelial Bladder Cancer Cells Undergo Metabolic Reprogramming beyond the Warburg Effect.Cancers · 2024Article
- Preclinical Evaluation of Zn(II) Self-Assemblies with Selective Cytotoxic Activity Against Cancer Cells In Vitro and In Ovo.Chemistry (Weinheim an der Bergstrasse, Germany) · 2024Article
- Sotorasib inhibits ubiquitination degradation of TXNIP and suppresses glucose metabolism inAmerican journal of cancer research · 2024Article
- Targeted therapies in bladder cancer: signaling pathways, applications, and challenges.MedComm · 2023Review
- Article
- One-Pot Analytical Pipeline for Efficient and Sensitive Proteomic Analysis of Extracellular Vesicles.Journal of proteome research · 2023Article
- Cross-species oncogenomics offers insight into human muscle-invasive bladder cancer.Genome biology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Bladder cancer is the 10th most common cancer worldwide. For muscle-invasive bladder cancer (MIBC), treatment includes radical cystectomy, radiotherapy, and chemotherapy; however, the outcome is generally poor. For non-muscle-invasive bladder cancer (NMIBC), tumor recurrence is common. There is an urgent need for more effective and less harmful therapeutic approaches. Here, bladder cancer cell metabolic reprogramming to rely on aerobic glycolysis (the Warburg effect) and expression of associated molecular therapeutic targets by bladder cancer cells of different stages and grades, and in freshly resected clinical tissue, is investigated. Importantly, analyses indicate that the Warburg effect is a feature of both NMIBCs and MIBCs. In two in vitro inducible epithelial-mesenchymal transition (EMT) bladder cancer models, EMT stimulation correlated with increased lactate production, the end product of aerobic glycolysis. Protein levels of lactate dehydrogenase A (LDH-A), which promotes pyruvate enzymatic reduction to lactate, were higher in most bladder cancer cell lines (compared with LDH-B, which catalyzes the reverse reaction), but the levels did not closely correlate with aerobic glycolysis rates. Although LDH-A is expressed in normal urothelial cells, LDH-A knockdown by RNAi selectively induced urothelial cancer cell apoptotic death, whereas normal cells were unaffected-identifying LDH-A as a cancer-selective therapeutic target for bladder cancers. LDH-A and other potential therapeutic targets (MCT4 and GLUT1) were expressed in patient clinical specimens; however, positive staining varied in different areas of sections and with distance from a blood vessel. This intratumoral heterogeneity has important therapeutic implications and indicates the possibility of tumor cell metabolic coupling.
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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.