ArticleBiophysical journal2015
Differential Redox Regulation of Ca²⁺ Signaling and Viability in Normal and Malignant Prostate Cells.
Article in Biophysical journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Crosstalk between calcium and reactive oxygen species signaling in cancer revisited.Cell calcium · 2025Review
- Modulatory Impact of Oxidative Stress on Action Potentials in Pathophysiological States: A Comprehensive Review.Antioxidants (Basel, Switzerland) · 2024Review
- Hydrogen peroxide disrupts the regulatory pathway of saliva secretion in two salivary acinar rat cell lines.Frontiers in molecular biosciences · 2024Article
- Malignant currents: sodium leak channel NALCN propels prostate cancer aggressiveness.The EMBO journal · 2023Article
- Calcium signalling pathways in prostate cancer initiation and progression.Nature reviews. Urology · 2023Review
- NNAT is a novel mediator of oxidative stress that suppresses ER + breast cancer.Molecular medicine (Cambridge, Mass.) · 2023Article
- Reactive Oxygen Species and Endothelial CaInternational journal of molecular sciences · 2021Review
- Arachidonic acid-regulated calcium signaling in T cells from patients with rheumatoid arthritis promotes synovial inflammation.Nature communications · 2021Article
- TRPM4 in Cancer-A New Potential Drug Target.Biomolecules · 2021Review
- Interrelation between ROS and CaRedox biology · 2020Review
- The Number and Position of Orai3 Units within Heteromeric Store-Operated CaInternational journal of molecular sciences · 2020Article
- Ultrasensitive System for Electrophysiology of Cancer Cell Populations: A Review.Bioelectricity · 2019Article
- Review
- Extracellular Electrophysiology in the Prostate Cancer Cell Model PC-3.Sensors (Basel, Switzerland) · 2019Article
- The role of the mitochondrial calcium uniporter (MCU) complex in cancer.Pflugers Archiv : European journal of physiology · 2018Review
- Crosstalk between calcium and reactive oxygen species signaling in cancer.Cell calcium · 2017Review
- Store-Operated CaCurrent molecular biology reports · 2017Review
- Thiol dependent intramolecular locking of Orai1 channels.Scientific reports · 2016Article
- The role of Orai-STIM calcium channels in melanocytes and melanoma.The Journal of physiology · 2016Review
- Regulation of Ca(2+) signaling in prostate cancer cells.Channels (Austin, Tex.) · 2016Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In prostate cancer, reactive oxygen species (ROS) are elevated and Ca(2+) signaling is impaired. Thus, several novel therapeutic strategies have been developed to target altered ROS and Ca(2+) signaling pathways in prostate cancer. Here, we investigate alterations of intracellular Ca(2+) and inhibition of cell viability caused by ROS in primary human prostate epithelial cells (hPECs) from healthy tissue and prostate cancer cell lines (LNCaP, DU145, and PC3). In hPECs, LNCaP and DU145 H2O2 induces an initial Ca(2+) increase, which in prostate cancer cells is blocked at high concentrations of H2O2. Upon depletion of intracellular Ca(2+) stores, store-operated Ca(2+) entry (SOCE) is activated. SOCE channels can be formed by hexameric Orai1 channels; however, Orai1 can form heteromultimers with its homolog, Orai3. Since the redox sensor of Orai1 (Cys-195) is absent in Orai3, the Orai1/Orai3 ratio in T cells determines the redox sensitivity of SOCE and cell viability. In prostate cancer cells, SOCE is blocked at lower concentrations of H2O2 compared with hPECs. An analysis of data from hPECs, LNCaP, DU145, and PC3, as well as previously published data from naive and effector TH cells, demonstrates a strong correlation between the Orai1/Orai3 ratio and the SOCE redox sensitivity and cell viability. Therefore, our data support the concept that store-operated Ca(2+) channels in hPECs and prostate cancer cells are heteromeric Orai1/Orai3 channels with an increased Orai1/Orai3 ratio in cells derived from prostate cancer tumors. In addition, ROS-induced alterations in Ca(2+) signaling in prostate cancer cells may contribute to the higher sensitivity of these cells to ROS.
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