ArticleCancer biology & therapy2010
Downregulation of voltage-dependent anion channel-1 expression by RNA interference prevents cancer cell growth in vivo.
Article in Cancer biology & therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Gene expression meta-analysis identifies VDAC1 as a predictor of poor outcome in early stage non-small cell lung cancer.PloS one · 2011Pooled it
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- Decoding Cancer through Silencing the Mitochondrial Gatekeeper VDAC1.Biomolecules · 2024Review
- The expression ofFrontiers in endocrinology · 2024Article
- Overexpression of the mitochondrial anti-viral signaling protein, MAVS, in cancers is associated with cell survival and inflammation.Molecular therapy. Nucleic acids · 2023Article
- Apoptotic proteins with non-apoptotic activity: expression and function in cancer.Apoptosis : an international journal on programmed cell death · 2023Review
- Pro-Apoptotic and Anti-Cancer Activity of the Vernonanthura Nudiflora Hydroethanolic Extract.Cancers · 2023Article
- Silencing VDAC1 to Treat Mesothelioma Cancer: Tumor Reprograming and Altering Tumor Hallmarks.Biomolecules · 2022Article
- Chloride Channels and Transporters: Roles beyond Classical Cellular Homeostatic pH or Ion Balance in Cancers.Cancers · 2022Review
- Pan-Cancer Analysis of Voltage-Dependent Anion Channel (VDAC1) as a Cancer Therapeutic Target or Diagnostic Biomarker.Disease markers · 2022Article
- VDAC1 Silencing in Cancer Cells Leads to Metabolic Reprogramming That Modulates Tumor Microenvironment.Cancers · 2021Article
- A Calcium Guard in the Outer Membrane: Is VDAC a Regulated Gatekeeper of Mitochondrial Calcium Uptake?International journal of molecular sciences · 2021Review
- Adverse Effects of Metformin From Diabetes to COVID-19, Cancer, Neurodegenerative Diseases, and Aging: Is VDAC1 a Common Target?Frontiers in physiology · 2021Review
- VDAC Genes Expression and Regulation in Mammals.Frontiers in physiology · 2021Review
- VDAC1 at the Intersection of Cell Metabolism, Apoptosis, and Diseases.Biomolecules · 2020Review
- The Mitochondrial Protein VDAC1 at the Crossroads of Cancer Cell Metabolism: The Epigenetic Link.Cancers · 2020Article
- Article
- Targeting Liver Cancer and Associated Pathologies in Mice with a Mitochondrial VDAC1-Based Peptide.Neoplasia (New York, N.Y.) · 2018Article
- VDAC1 at the crossroads of cell metabolism, apoptosis and cell stress.Cell stress · 2017Article
- VDAC1 is a molecular target in glioblastoma, with its depletion leading to reprogrammed metabolism and reversed oncogenic properties.Neuro-oncology · 2017Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The voltage-dependent anion channel 1 (VDAC1), located at the outer mitochondrial membrane (OMM), is a key protein in regulating the exchange of ions, nucleotides and a variety of metabolites in and out of the mitochondria. As such, VDAC serves a crucial role in cellular energy maintenance. We have previously shown that silencing VDAC1 expression in T-Rex-293 cells by means of RNA interference using shRNA directed to human (h)VDAC1 resulted in reduced ATP production and a decrease in cell growth. Since cancer cells highly express VDAC, we examined here the effects of shRNA-hVDAC1-mediated silencing of VDAC1 expression on cancer cell growth in an animal model. To this end, HeLa cervical cancer cells were stably transfected with an inducible shRNA plasmid encoding for a sequence directed to hVDAC1. VDAC1 expression in these cells was decreased almost completely. Stably transfected shRNA-hVDAC1 HeLa cells proliferated much slower than did control cells, pointing to VDAC1 expression as being essential for normal growth of HeLa cancer cells. We further studied the ability of hVDAC1 silencing to block cancer cell proliferation in vivo. Nude mice subcutaneously inoculated with stably transfected shRNA-hVDAC1 HeLa cells developed about 40-fold smaller tumors than did mice inoculated with control HeLa cells. Taken together, the results of this study demonstrate, for the first time, the anticancer therapeutic potential of VDAC1 downregulation by means of shRNA.
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