ArticleJournal of cellular and molecular medicine2012
Epigallocatechin-3-gallate induces mesothelioma cell death via H2 O2 -dependent T-type Ca2+ channel opening.
Article in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
- Umbilical Cord PRP Accelerates Corneal Wound Healing via AQP1 Upregulation and Calcium Signaling.Biology · 2026Article
- Unraveling BOLD-100 synergistic potential in pleural mesothelioma treatment: an in vitro study.Investigational new drugs · 2025Article
- Computer-Aided Discovery of Natural Compounds Targeting the ADAR2 dsRBD2-RNA Interface and Computational Modeling of Full-Length ADAR2 Protein Structure.International journal of molecular sciences · 2025Article
- Thonzonium bromide inhibits progression of malignant pleural mesothelioma through regulation of ERK1/2 and p38 pathways and mitochondrial uncoupling.Cancer cell international · 2024Article
- Predicting survival for patients with mesothelioma: development of the PLACE prognostic model.BMC cancer · 2023Article
- Prognostic significance of inflammation-related and electrolyte laboratory variables in patients with malignant pleural mesothelioma.Frontiers in medicine · 2023Article
- Article
- Green Tea Polyphenol (-)-Epigallocatechin-3-Gallate (EGCG): A Time for a New Player in the Treatment of Respiratory Diseases?Antioxidants (Basel, Switzerland) · 2022Review
- Inhibition of Cell Proliferation and Cell Viability by Sinecatechins in Cutaneous SCC Cells Is Related to an Imbalance of ROS and Loss of Mitochondrial Membrane Potential.Antioxidants (Basel, Switzerland) · 2022Article
- EGCG Enhances the Chemosensitivity of Colorectal Cancer to Irinotecan through GRP78-MediatedEndoplasmic Reticulum Stress.Journal of oncology · 2022Article
- Cancer Therapy Challenge: It Is Time to Look in the "St. Patrick's Well" of the Nature.International journal of molecular sciences · 2021Review
- Phytochemicals in Malignant Pleural Mesothelioma Treatment-Review on the Current Trends of Therapies.International journal of molecular sciences · 2021Review
- Flow Cytofluorometric Analysis of Molecular Mechanisms of Premature Red Blood Cell Death.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Manuka Honey Induces Apoptosis of Epithelial Cancer Cells through Aquaporin-3 and Calcium Signaling.Life (Basel, Switzerland) · 2020Article
- Endothelial response boosted by platelet lysate: the involvement of calcium toolkit.International journal of molecular sciences · 2020Article
- Targeting Calcium Signalling in Malignant Mesothelioma.Cancers · 2019Review
- Neuroprotective and Anti-Amyloid β Effect and Main Chemical Profiles of White Tea: Comparison Against Green, Oolong and Black Tea.Molecules (Basel, Switzerland) · 2019Article
- Propolis Induces AQP3 Expression: A Possible Way of Action in Wound Healing.Molecules (Basel, Switzerland) · 2019Article
- Honey-Mediated Wound Healing: H₂O₂ Entry through AQP3 Determines Extracellular CaInternational journal of molecular sciences · 2019Article
- The Potential Protective Effects of Polyphenols in Asbestos-Mediated Inflammation and Carcinogenesis of Mesothelium.Nutrients · 2016Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant mesothelioma (MMe) is a highly aggressive, lethal tumour requiring the development of more effective therapies. The green tea polyphenol epigallocathechin-3-gallate (EGCG) inhibits the growth of many types of cancer cells. We found that EGCG is selectively cytotoxic to MMe cells with respect to normal mesothelial cells. MMe cell viability was inhibited by predominant induction of apoptosis at lower doses and necrosis at higher doses. EGCG elicited H(2) O(2) release in cell cultures, and exogenous catalase (CAT) abrogated EGCG-induced cytotoxicity, apoptosis and necrosis. Confocal imaging of fluo 3-loaded, EGCG-exposed MMe cells showed significant [Ca(2+) ](i) rise, prevented by CAT, dithiothreitol or the T-type Ca(2+) channel blockers mibefradil and NiCl(2) . Cell loading with dihydrorhodamine 123 revealed EGCG-induced ROS production, prevented by CAT, mibefradil or the Ca(2+) chelator BAPTA-AM. Direct exposure of cells to H(2) O(2) produced similar effects on Ca(2+) and ROS, and these effects were prevented by the same inhibitors. Sensitivity of REN cells to EGCG was correlated with higher expression of Ca(v) 3.2 T-type Ca(2+) channels in these cells, compared to normal mesothelium. Also, Ca(v) 3.2 siRNA on MMe cells reduced in vitro EGCG cytotoxicity and abated apoptosis and necrosis. Intriguingly, Ca(v) 3.2 expression was observed in malignant pleural mesothelioma biopsies from patients, but not in normal pleura. In conclusion, data showed the expression of T-type Ca(2+) channels in MMe tissue and their role in EGCG selective cytotoxicity to MMe cells, suggesting the possible use of these channels as a novel MMe pharmacological target.
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