ArticleAmerican journal of physiology. Cell physiology2013
Role of TRPM2 in cell proliferation and susceptibility to oxidative stress.
Article in American journal of physiology. Cell physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- PARP1-TRPM2-PKC cascade distinctly regulates reactive astrogliosis and clasmatodendrosis through NF-κB and AKT pathways in the hippocampus of chronic epilepsy rats.Scientific reports · 2025Article
- Ion channel mutations and cancer.Biochemistry and biophysics reports · 2025Review
- Crosstalk between calcium and reactive oxygen species signaling in cancer revisited.Cell calcium · 2025Review
- Nitroxidative Stress, Cell-Signaling Pathways, and Manganese Porphyrins: Therapeutic Potential in Neuropathic Pain.International journal of molecular sciences · 2025Review
- Unlocking the potential of cardiac TRP channels using knockout mice models.Frontiers in physiology · 2025Article
- TRPM channels in human cancers: regulatory mechanism and therapeutic prospects.Biomarker research · 2024Review
- TRPM2 knockdown attenuates myocardial apoptosis and promotes autophagy in HFD/STZ-induced diabetic mice via regulating the MEK/ERK and mTORC1 signaling pathway.Molecular and cellular biochemistry · 2024Article
- High-throughput screening of transient receptor potential (TRP) channels in pterygium.International ophthalmology · 2024Article
- Bidirectional regulation mechanism of TRPM2 channel: role in oxidative stress, inflammation and ischemia-reperfusion injury.Frontiers in immunology · 2024Review
- TRP Channels in Cancer: Signaling Mechanisms and Translational Approaches.Biomolecules · 2023Review
- Identification of TRPM2 as a prognostic factor correlated with immune infiltration in ovarian cancer.Journal of ovarian research · 2023Article
- TRPM2 Channels: A Potential Therapeutic Target in Melanoma?International journal of molecular sciences · 2023Review
- TRPM2-mediated CaCell communication and signaling : CCS · 2023Review
- Cell death induction and protection by activation of ubiquitously expressed anion/cation channels. Part 3: the roles and properties of TRPM2 and TRPM7.Frontiers in cell and developmental biology · 2023Review
- The human ion channel TRPM2 modulates migration and invasion in neuroblastoma through regulation of integrin expression.Scientific reports · 2022Article
- The Janus-faced role of TRPM2-S in retroperitoneal liposarcoma via increasing ROS levels.Cell communication and signaling : CCS · 2022Article
- Mutations in calmodulin-binding domains of TRPV4/6 channels confer invasive properties to colon adenocarcinoma cells.Channels (Austin, Tex.) · 2020Article
- Roles of NADMolecules (Basel, Switzerland) · 2020Review
- Resveratrol attenuates hypoxia-induced neuronal cell death, inflammation and mitochondrial oxidative stress by modulation of TRPM2 channel.Scientific reports · 2020Article
- Long non-coding RNAs regulate drug resistance in cancer.Molecular cancer · 2020Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The transient receptor potential (TRP) channel TRPM2 is an ion channel that modulates cell survival. We report here that full-length (TRPM2-L) and short (TRPM2-S) isoform expression was significantly increased in human neuroblastoma compared with adrenal gland. To differentiate the roles of TRPM2-L and TRPM2-S in cell proliferation and survival, we established neuroblastoma SH-SY5Y cell lines stably expressing either TRPM2 isoform or empty vector. Cells expressing TRPM2-S showed significantly enhanced proliferation, downregulation of phosphatase and tensin homolog (PTEN), and increased protein kinase B (Akt) phosphorylation and cell surface glucose transporter 1 (Glut1) compared with cells expressing TRPM2-L or empty vector. ERK phosphorylation was increased, and forkhead box O 3a (FOXO3a) levels were decreased. Inhibitor studies demonstrated that enhanced proliferation was dependent on phosphatidylinositol 3-kinase/Akt, ERK, and NADPH oxidase activation. On the other hand, TRPM2-S-expressing cells were significantly more susceptible to cell death induced by low H2O2 concentrations (50-100 μM), whereas TRPM2-L-expressing cells were protected. This was associated with a significant increase in FOXO3a, MnSOD (SOD2), and membrane Glut1 in TRPM2-L-expressing cells compared with TRPM2-S expressing cells. We conclude that TRPM2 channels occupy a key role in cell proliferation and survival following oxidative stress in neuroblastoma. Our results suggest that overexpression of TRPM2-S results in increased proliferation through phosphatidylinositol 3-kinase/Akt and ERK pathways, while overexpression of TRPM2-L confers protection against oxidative stress-induced cell death through FOXO3a and SOD. TRPM2 channels may represent a novel future therapeutic target in diseases involving oxidative stress.
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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.