ArticleCells2019
TTYH1 and TTYH2 Serve as LRRC8A-Independent Volume-Regulated Anion Channels in Cancer Cells.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Identification of metabolism-associated molecular classification and prognostic genes for medulloblastoma based on bioinformatics analysis.Clinics (Sao Paulo, Brazil) · 2026Article
- Identification of prognostic biomarkers associated with T and melanoma cell subpopulations in melanoma through integrating machine learning and multiomics.Discover oncology · 2025Article
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- KPNA2 promotes the progression of gastric cancer by regulating the alternative splicing of related genes.Scientific reports · 2024Article
- Prominin 1 and Tweety Homology 1 both induce extracellular vesicle formation.bioRxiv : the preprint server for biology · 2024Article
- Investigation of Glycosylphosphatidylinositol (GPI)-Plasma Membrane Interaction in Live Cells and the Influence of GPI Glycan Structure on the Interaction.Chemistry (Weinheim an der Bergstrasse, Germany) · 2024Article
- Article
- Physiology of the volume-sensitive/regulatory anion channel VSOR/VRAC. Part 1: from its discovery and phenotype characterization to the molecular entity identification.The journal of physiological sciences : JPS · 2024Review
- Approach for Elucidating the Molecular Mechanism of Epithelial to Mesenchymal Transition in Fibrosis of Asthmatic Airway Remodeling Focusing on ClInternational journal of molecular sciences · 2023Review
- Review
- Deficiency of TTYH1 Expression Reduces the Migration and Invasion of U2OS Human Osteosarcoma Cells.Life (Basel, Switzerland) · 2022Article
- The Role of Chloride Channels in the Multidrug Resistance.Membranes · 2021Review
- Cloning and Functional Analysis of Rat Tweety-Homolog 1 Gene Promoter.Neurochemical research · 2021Article
- Cryo-EM structures of the TTYH family reveal a novel architecture for lipid interactions.Nature communications · 2021Article
- Tweety-Homolog 1 Facilitates Pain via Enhancement of Nociceptor Excitability and Spinal Synaptic Transmission.Neuroscience bulletin · 2021Article
- Elevated expression of Tweety homologue 3 predicts poor clinical outcomes in ovarian cancer.Journal of Cancer · 2021Article
- TheFrontiers in molecular neuroscience · 2021Article
- Transmembrane Protein Ttyh1 Maintains the Quiescence of Neural Stem Cells Through CaFrontiers in cell and developmental biology · 2021Article
- Cell Death Induction and Protection by Activation of Ubiquitously Expressed Anion/Cation Channels. Part 1: Roles of VSOR/VRAC in Cell Volume Regulation, Release of Double-Edged Signals and Apoptotic/Necrotic Cell Death.Frontiers in cell and developmental biology · 2020Review
- Acid- and Volume-Sensitive Chloride Currents in Human Chondrocytes.Frontiers in cell and developmental biology · 2020Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Volume-regulated anion channels (VRACs) are involved in cellular functions such as regulation of cell volume, proliferation, migration, and cell death. Although leucine-rich repeat-containing 8A (LRRC8A) has been characterized as a molecular component of VRACs, here we show that Drosophila melanogaster tweety homologue 1 and 2 (TTYH1 and TTYH2) are critical for VRAC currents in cancer cells. LRRC8A-independent VRAC currents were present in the gastric cancer cell line SNU-601, but almost completely absent in its cisplatin-resistant derivative SNU-601-R10 (R10). The VRAC current in R10 was partially restored by treatment with trichostatin A (TSA), a histone deacetylase inhibitor. Based on microarray expression profiling of these cells, we selected two chloride channels, TTYH1 and TTYH2, as VRAC candidates. VRAC currents were completely absent from TTYH1- and TTYH2-deficient SNU-601 cells, and were clearly restored by expression of TTYH1 or TTYH2. In addition, we examined the expression of TTYH1 or TTYH2 in several cancer cell lines and found that VRAC currents of these cells were abolished by gene silencing of TTYH1 or TTYH2. Taken together, our data clearly show that TTYH1 and TTYH2 can act as LRRC8A-independent VRACs, suggesting novel therapeutic approaches for VRACs in cancer cells.
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