ArticleCell death discovery2024
BAP1 inactivation promotes lactate production by leveraging the subcellular localization of LDHA in melanoma.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed.
- Metabolic reprogramming via LDHB confers resistance to lactate-induced dysfunction and enhanced antitumor activity in hiPSC-Derived NK cells.Stem cell reports · 2026Article
- Redox Homeostasis, Metabolic Pathways and Plasticity in Uveal Melanoma Compared to Other Cancers.Cancers · 2026Review
- Metabolic Regulation of Immune Responses: Molecular Mechanisms, Diseases, and Therapeutic Targets.MedComm · 2026Review
- E3 ubiquitin ligase RNF40: Structure, function and its context‑dependent roles in tumorigenesis (Review).Oncology reports · 2026Review
- Targeting KIF20A blocks lactylation modification to suppress immune escape in hepatocellular carcinoma.iScience · 2026Article
- Focus on Lactate and Lactylation Modification: The Potential Role in Ophthalmic Disease Treatment.International journal of molecular sciences · 2026Review
- Tumor microenvironment-driven drug resistance in urologic cancers: mechanisms and therapeutic targets.Genes & genomics · 2026Review
- GLUT1 expression, lymphocyte distribution and CD3Journal of experimental & clinical cancer research : CR · 2026Article
- Tumor suppressor BAP1 emerges as a key regulator of metabolism and cell death in tumors.Frontiers in cell and developmental biology · 2026Review
- Integrating multiple key molecules in uveal melanoma to uncover metastatic and immune microenvironment-related gene signatures.International journal of ophthalmology · 2026Article
- Identification and mechanism analysis of biomarkers related to butyrate metabolism in COVID-19 patients.Annals of medicine · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
BRCA1-associated protein 1 (BAP1) acts as a tumor suppressor and can affect the cell cycle, tumor immunity, and cellular metabolism through multiple pathways. In melanoma, BAP1 mutations promote tumor cell glycolysis, leading to increased lactate production. The tumor microenvironment with high lactate levels is often associated with immunosuppression and tumor progression. The inhibitory effect of BAP1 on glycolysis has been found in a variety of tumors, but the specific mechanism by which BAP1 inhibits lactate production still needs to be elucidated. In this study, we show that BAP1 can interact directly with lactate dehydrogenase (LDHA), causing LDHA to accumulate in the nucleus. Conversely, BAP1 deletion leads to the accumulation of LDHA in the cytoplasm, catalyzing the production of lactate from pyruvate that results in increased lactate levels inside and outside the cell. By elucidating the interaction between BAP1 and LDHA and the subsequent effects on lactate production in melanoma cells, this work provides insights into the mechanism of BAP1-mediated metabolic regulation. Furthermore, it may provide novel directions for the clinical treatment of BAP1-mutant melanoma.
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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.