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• W2771060572 abstract "The transient receptor potential melastatin 2 (TRPM2) ion channel has an essential function in modulating cell survival following oxidant injury and is highly expressed in many cancers including neuroblastoma. To study the function of TRPM2 in cancer cell growth, TRPM2 was inhibited with the dominant negative short splice variant TRPM2-S or depleted in SH-SY5Y neuroblastoma cells with CRISPR technology. Inhibition of TRPM2 with TRPM2-S or depletion in neuroblastoma cells significantly decreased tumor growth in xenograft models and increased sensitivity to doxorubicin in cell culture, demonstrating the important role of TRPM2-mediated calcium entry. To examine the mechanism, expression of HIF-1/2α, which can be regulated by calcium dependent processes, was studied. HIF-1/2α expression and that of downstream proteins regulated by HIF-1/2α were reduced in TRPM2 inhibited cells, including proteins involved in glycolysis, mitochondrial electron transport chain activity (complex I, NDUFA4L2; complex IV, cytochrome oxidase 4.1/4.2), mitophagy (BNIP3), and antioxidants (SOD1/2, FOXO3a). Mitochondrial membrane potential, oxygen consumption rate, and ATP production were significantly decreased in TRPM2 inhibited or depleted cells. Expression of the NF-E2-related factor 2 (Nrf2) and downstream antioxidant enzymes were also significantly decreased in TRPM2 depleted cells. This was associated with a significant reduction in glutathione (GSH) and NADPH. Together, the decrease in mitochondrial electron transport chain proteins and the decrease in anti-oxidant enzymes resulted in a significantly increased mitochondrial and cellular ROS levels. These data show that expression and activity of TRPM2 are important for mitochondrial function, cellular bioenergetics, and modulation of ROS. In TRPM2 depleted cells, oxidant stress is increased, both by higher ROS production and lower levels of HIF-1α, Nrf2, GSH, and NADPH. Inhibition of TRPM2 is a novel therapeutic approach to target tumor cells and increase susceptibility to chemotherapy agents through increased ROS and impaired energy production." @default.
• W2771060572 created "2017-12-04" @default.
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• W2771060572 date "2017-11-01" @default.
• W2771060572 modified "2023-10-14" @default.
• W2771060572 title "Role Of The Ca 2+ Channel TRPM2 In Regulation Of Oxidative Stress And Energy Balance" @default.
• W2771060572 doi "https://doi.org/10.1016/j.freeradbiomed.2017.10.361" @default.
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