ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2016
Resveratrol Specifically Kills Cancer Cells by a Devastating Increase in the Ca2+ Coupling Between the Greatly Tethered Endoplasmic Reticulum and Mitochondria.
Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 99 citations in OpenAlex.
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- Antitumor natural products targeting mitochondrial NADH: ubiquinone oxidoreductase (complex I): a review.Frontiers in pharmacology · 2026Review
- Enhancing Late-Life Survival and Mobility via Mitohormesis by Reducing Mitochondrial Calcium Levels.Aging cell · 2025Article
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- Kinase signalling adaptation supports dysfunctional mitochondria in disease.Frontiers in molecular biosciences · 2024Review
- Nano-modulators with the function of disrupting mitochondrial CaJournal of nanobiotechnology · 2023Article
- Anti-Cancer Properties of Resveratrol: A Focus on Its Impact on Mitochondrial Functions.Antioxidants (Basel, Switzerland) · 2023Review
- Phytochemical Targeting of Mitochondria for Breast Cancer Chemoprevention, Therapy, and Sensitization.International journal of molecular sciences · 2022Review
- Natural Polyphenols as SERCA Activators: Role in the Endoplasmic Reticulum Stress-Related Diseases.Molecules (Basel, Switzerland) · 2022Review
- Citrin mediated metabolic rewiring in response to altered basal subcellular CaCommunications biology · 2022Article
- Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction.Frontiers in cell and developmental biology · 2022Review
- Protodioscin Induces Mitochondrial Apoptosis of Human Hepatocellular Carcinoma Cells Through Eliciting ER Stress-Mediated IP3R Targeting Mfn1/Bak Expression.Journal of hepatocellular carcinoma · 2022Article
- Biomolecular Evaluation of Piceatannol's Effects in Counteracting the Senescence of Mesenchymal Stromal Cells: A New Candidate for Senotherapeutics?International journal of molecular sciences · 2021Article
- Clinical significance of P-class pumps in cancer.Oncology letters · 2021Review
- Protective Effect of Piceatannol Against Cerebral Ischaemia-Reperfusion Injury Via Regulating Nrf2/HO-1 Pathway In Vivo and Vitro.Neurochemical research · 2021Article
- Mitochondrial CaCells · 2021Review
- Piceatannol-Loaded Bilosome-Stabilized Zein Protein Exhibits Enhanced Cytostatic and Apoptotic Activities in Lung Cancer Cells.Pharmaceutics · 2021Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND/
aimsResveratrol and its derivate piceatannol are known to induce cancer cell-specific cell death. While multiple mechanisms of actions have been described including the inhibition of ATP synthase, changes in mitochondrial membrane potential and ROS levels, the exact mechanisms of cancer specificity of these polyphenols remain unclear. This paper is designed to reveal the molecular basis of the cancer-specific initiation of cell death by resveratrol and piceatannol.
methodsThe two cancer cell lines EA.hy926 and HeLa, and somatic short-term cultured HUVEC were used. Cell viability and caspase 3/7 activity were tested. Mitochondrial, cytosolic and endoplasmic reticulum Ca2+ as well as cytosolic and mitochondrial ATP levels were measured using single cell fluorescence microscopy and respective genetically-encoded sensors. Mitochondria-ER junctions were analyzed applying super-resolution SIM and ImageJ-based image analysis.
resultsResveratrol and piceatannol selectively trigger death in cancer but not somatic cells. Hence, these polyphenols strongly enhanced mitochondrial Ca2+ uptake in cancer exclusively. Resveratrol and piceatannol predominantly affect mitochondrial but not cytosolic ATP content that yields in a reduced SERCA activity. Decreased SERCA activity and the strongly enriched tethering of the ER and mitochondria in cancer cells result in an enhanced MCU/Letm1-dependent mitochondrial Ca2+ uptake upon intracellular Ca2+ release exclusively in cancer cells. Accordingly, resveratrol/piceatannol-induced cancer cell death could be prevented by siRNA-mediated knock-down of MCU and Letm1.
conclusionsBecause their greatly enriched ER-mitochondria tethering, cancer cells are highly susceptible for resveratrol/piceatannol-induced reduction of SERCA activity to yield mitochondrial Ca2+ overload and subsequent cancer cell death.
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