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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/111492


    Title: Heme oxygenase-1 mediates BAY 11-7085 induced ferroptosis.
    Authors: LC, Chang;LC, Chang;*;SK, Chiang;SK, Chiang;SE, Chen;SE, Chen;余永倫;鄒瑞煌;WC, Chang;WC, Chang
    Contributors: 生物科技學系
    Date: 2018-03
    Issue Date: 2018-10-16 14:49:41 (UTC+8)
    Abstract: Ferroptosis is a form of oxidative cell death and has become a chemotherapeutic target for cancer treatment. BAY 11–7085 (BAY), which is a well-known IκBα inhibitor, suppressed viability in cancer cells via induction of ferroptotic death in an NF-κB-independent manner. Reactive oxygen species scavenging, relief of lipid peroxidation, replenishment of glutathione and thiol-containing agents, as well as iron chelation, rescued BAY-induced cell death. BAY upregulated a variety of Nrf2 target genes related to redox regulation, particularly heme oxygenase-1 (HO-1). Studies with specific inhibitors and shRNA interventions suggested that the hierarchy of induction is Nrf2−SLC7A11−HO-1. SLC7A11 inhibition by erastin, sulfasalazine, or shRNA interference sensitizes BAY-induced cell death. Overexperession of SLC7A11 attenuated BAY-inhibited cell viability. The ferroptotic process induced by hHO-1 overexpression further indicated that HO-1 is a key mediator of BAY-induced ferroptosis that operates through cellular redox regulation and iron accumulation. BAY causes compartmentalization of HO-1 into the nucleus and mitochondrion, and followed mitochondrial dysfunctions, leading to lysosome targeting for mitophagy. In this study, we first discovered that BAY induced ferroptosis via Nrf2−SLC7A11−HO-1 pathway and HO-1 is a key mediator by responding to the cellular redox status.
    Relation: CANCER LETTERS
    Appears in Collections:[生物科技學系] 期刊論文

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