ArticleOxidative medicine and cellular longevity2016
Targeting TRPM2 Channels Impairs Radiation-Induced Cell Cycle Arrest and Fosters Cell Death of T Cell Leukemia Cells in a Bcl-2-Dependent Manner.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 67 citations in OpenAlex.
- Review
- TRPM2: a pivotal player in tumor progression and a promising therapeutic target.Cancer cell international · 2025Review
- Sodium Chloride Nanoparticles Potentiate Radiation Therapy by Disrupting Osmolarity Balance and Enhancing Antitumor Immunity.Nano letters · 2025Article
- Review
- Ectopically expressed rhodopsin is not sensitive to X-rays.BMC neuroscience · 2024Article
- Advances in the role of ion channels in leukemia.Heliyon · 2024Review
- Identification of TRPM2 as a prognostic factor correlated with immune infiltration in ovarian cancer.Journal of ovarian research · 2023Article
- TRP Channels in Tumoral Processes Mediated by Oxidative Stress and Inflammation.Antioxidants (Basel, Switzerland) · 2023Review
- TRPM2-mediated CaCell communication and signaling : CCS · 2023Review
- The human ion channel TRPM2 modulates migration and invasion in neuroblastoma through regulation of integrin expression.Scientific reports · 2022Article
- Pan-cancer analyses reveal the genetic and pharmacogenomic landscape of transient receptor potential channels.NPJ genomic medicine · 2022Article
- The human ion channel TRPM2 modulates cell survival in neuroblastoma through E2F1 and FOXM1.Scientific reports · 2022Article
- The regulatory and modulatory roles of TRP family channels in malignant tumors and relevant therapeutic strategies.Acta pharmaceutica Sinica. B · 2022Review
- Targeting Ion Channels for Cancer Treatment: Current Progress and Future Challenges.Reviews of physiology, biochemistry and pharmacology · 2022Review
- On the modulation of TRPM channels: Current perspectives and anticancer therapeutic implications.Frontiers in oncology · 2022Review
- Deregulated calcium signaling in blood cancer: Underlying mechanisms and therapeutic potential.Frontiers in oncology · 2022Review
- Brain Damage and Patterns of Neurovascular Disorder after Ionizing Irradiation. Complications in Radiotherapy and Radiation Combined Injury.Radiation research · 2021Review
- TRPM2 promotes pancreatic cancer by PKC/MAPK pathway.Cell death & disease · 2021Article
- Transient Receptor Potential (TRP) Channels in Haematological Malignancies: An Update.Biomolecules · 2021Review
- Identification of TRPM2 as a Marker Associated With Prognosis and Immune Infiltration in Kidney Renal Clear Cell Carcinoma.Frontiers in molecular biosciences · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Messenger RNA data of lymphohematopoietic cancer lines suggest a correlation between expression of the cation channel TRPM2 and the antiapoptotic protein Bcl-2. The latter is overexpressed in various tumor entities and mediates therapy resistance. Here, we analyzed the crosstalk between Bcl-2 and TRPM2 channels in T cell leukemia cells during oxidative stress as conferred by ionizing radiation (IR). To this end, the effects of TRPM2 inhibition or knock-down on plasma membrane currents, Ca(2+) signaling, mitochondrial superoxide anion formation, and cell cycle progression were compared between irradiated (0-10 Gy) Bcl-2-overexpressing and empty vector-transfected Jurkat cells. As a result, IR stimulated a TRPM2-mediated Ca(2+)-entry, which was higher in Bcl-2-overexpressing than in control cells and which contributed to IR-induced G2/M cell cycle arrest. TRPM2 inhibition induced a release from G2/M arrest resulting in cell death. Collectively, this data suggests a pivotal function of TRPM2 in the DNA damage response of T cell leukemia cells. Apoptosis-resistant Bcl-2-overexpressing cells even can afford higher TRPM2 activity without risking a hazardous Ca(2+)-overload-induced mitochondrial superoxide anion formation.
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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.