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Heme oxygenase-1 Mediates BAY 11-7085 Induced Ferroptosis

Heme oxygenase-1 Mediates BAY 11-7085 Induced Ferroptosis

Ling-Chu Chang, Shih-Kai Chiang, Shuen-Ei Chen, Yung-Luen Yu, Ruey-Hwang Chou, Wei-Chao Chang

Cancer Lett. 2018 Mar 1;416:124-137.

PMID: 29274359

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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP196309769	Bay 11-7085		196309-76-9	Price

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