ReviewFrontiers in physiology2021
VDAC Modulation of Cancer Metabolism: Advances and Therapeutic Challenges.
Review in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 56 citations in OpenAlex.
- Mitochondrial Fitness as a Functional Immune Checkpoint in Cancer: Metabolic Plasticity, Tumor Evolution, and Immunotherapy.Cancers · 2026Review
- Review
- Research progress on VDAC2 in mitochondrial dysfunction-related diseases.Molecular biology reports · 2026Review
- Elliptical β-barrel deformation underlies gating in VDAC1.Protein science : a publication of the Protein Society · 2026Article
- Small molecule inhibition of voltage dependent anion channel 1 reroutes mitochondrial metabolite flux.Molecules and cells · 2026Article
- Article
- Anti-cancer drugs targeting the NADH-binding site of VDAC rewire channel electrophysiology and partially suppress cation selectivity.The FEBS journal · 2026Article
- The compartment-specific interactome of VDAC1 reveals its emerging role beyond mitochondria in breast cancer.Scientific reports · 2026Article
- Targeting ion channel dysregulation in tumors: emerging therapeutic opportunities.Trends in pharmacological sciences · 2026Review
- Trim15 stabilizes VDAC3 via ubiquitination to suppress autophagy and enhance chemosensitivity in hypopharyngeal squamous cell carcinoma.Cell death discovery · 2026Article
- The cGAS-STING pathway and mitochondrial metabolism: from mechanistic insights to therapeutic potential in tumor.Journal of translational medicine · 2026Review
- Multiomics and Genomic Alteration Characterization Identifies VDAC1 as a Mitochondrial-Associated Biomarker in Pancreatic Cancer.Human mutation · 2026Article
- Mitochondrial gatekeeper in hepatocellular carcinoma: Unraveling the multifaceted roles of VDAC in metabolic reprogramming, apoptosis evasion and therapeutic innovation (Review).Molecular medicine reports · 2026Review
- Is the Voltage-Dependent Anion Channel a Major Player in Neurodegenerative Diseases?International journal of molecular sciences · 2025Review
- Exploring the Anti-Leukemic Effect of the Synthetic Retinoid ST1926 on Malignant T Cells: A Comprehensive Proteomics Approach.International journal of molecular sciences · 2025Article
- Mitochondrial pyruvate dehydrogenase phosphatase metabolism disorder in malignant tumors.Oncology research · 2025Review
- Modulation of mitochondrial voltage dependent anion channel: studies on bilayer electrophysiology.Frontiers in physiology · 2025Review
- Single-cell sensor analyses reveal signaling programs enabling Ras-G12C drug resistance.Nature chemical biology · 2025Article
- Facts, Dogmas, and Unknowns About Mitochondrial Reactive Oxygen Species in Cancer.Antioxidants (Basel, Switzerland) · 2024Review
- Developing a Novel and Optimized Yeast Model for Human VDAC Research.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Most anionic metabolites including respiratory substrates, glycolytic adenosine triphosphate (ATP), and small cations that enter mitochondria, and mitochondrial ATP moving to the cytosol, cross the outer mitochondrial membrane (OMM) through voltage dependent anion channels (VDAC). The closed states of VDAC block the passage of anionic metabolites, and increase the flux of small cations, including calcium. Consequently, physiological or pharmacological regulation of VDAC opening, by conditioning the magnitude of both anion and cation fluxes, is a major contributor to mitochondrial metabolism. Tumor cells display a pro-proliferative Warburg phenotype characterized by enhanced aerobic glycolysis in the presence of partial suppression of mitochondrial metabolism. The heterogeneous and flexible metabolic traits of most human tumors render cells able to adapt to the constantly changing energetic and biosynthetic demands by switching between predominantly glycolytic or oxidative phenotypes. Here, we describe the biological consequences of changes in the conformational state of VDAC for cancer metabolism, the mechanisms by which VDAC-openers promote cancer cell death, and the advantages of VDAC opening as a valuable pharmacological target. Particular emphasis is given to the endogenous regulation of VDAC by free tubulin and the effects of VDAC-tubulin antagonists in cancer cells. Because of its function and location, VDAC operates as a switch to turn-off mitochondrial metabolism (closed state) and increase aerobic glycolysis (pro-Warburg), or to turn-on mitochondrial metabolism (open state) and decrease glycolysis (anti-Warburg). A better understanding of the role of VDAC regulation in tumor progression is relevant both for cancer biology and for developing novel cancer chemotherapies.
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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.