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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/14463


    Title: CCAAT/enhancer-binding protein delta regulates glioblastoma survival through catalase-mediated hydrogen peroxide clearance
    Authors: Lin, HY;Lim, SW;Hsu, TI;Yang, WB;Huang, CC;Tsai, YT;Chang, WC;Ko, CY
    Contributors: NHRI Graduate Student Program
    Abstract: It has long been documented that cancer cells show increased and persistent oxidative stress due to increased reactive oxygen species (ROS), which is necessary for their increased proliferative rate. Due to the high levels of ROS, cancer cells also stimulate the antioxidant system, which includes the enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX), to eliminate ROS. However, overexpressed antioxidant enzymes often lead to drug resistance and therapeutic failure. Glioblastoma (GBM) is the most aggressive brain tumor and has the poorest prognosis. The transcription factor CCAAT/enhancer-binding protein delta (CEBPD) is highly expressed in GBM and correlates with drug resistance, prompting us to elucidate its role in GBM cell survival. In this study, we first demonstrated that loss of CEBPD significantly inhibited GBM cell viability and increased cell apoptosis. Furthermore, the expression of CAT was attenuated through promoter regulation following CEBPD knockdown, accelerating intracellular hydrogen peroxide (H(2)O(2)) accumulation. In addition, mitochondrial function was impaired in CEBPD knockdown cells. Together, we revealed the mechanism by which CEBPD-mediated CAT expression regulates H(2)O(2) clearance for GBM cell survival.
    Date: 2022-08-18
    Relation: Oxidative Medicine and Cellular Longevity. 2022 Aug 18;2022:Article number 4081380.
    Link to: http://dx.doi.org/10.1155/2022/4081380
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000848371000006
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85136893168
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