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HIF-1α-Mediated Mitophagy Determines ZnO Nanoparticle-Induced Human Osteosarcoma Cell Death both In Vitro and In Vivo by He, Guanping; Pan, Xiaoyu; Liu, Xiao; Zhu, Ye; Ma, Yunlong; Du, Chuanchao; Liu, Xiaoguang; Mao, Chuanbin is a Engineering article available to read on EtoBox.

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Although ZnO nanoparticles (NPs) can kill human osteosarcoma cells, the underlying upstream regulatory mechanisms remain unclear. Since hypoxia inducible factor-1α (HIF-1α) regulates the tumor microenvironment, here we explored the interplay between HIF-1α regulation and mitophagy in ZnO NP-induced osteosarcoma inhibition both in vivo and in vitro. We found that ZnO NPs upregulated HIF-1α protein levels when they killed four common human osteosarcoma cell lines. This finding was consistent with our observations that additional HIF-1α upregulation by a hypoxia inducer CoCl or under a 1% hypoxia environment enhanced NP-induced cell death, but concurrent HIF-1α suppression by a hypoxia inhibitor YC-1 or HIF-1α siRNA inhibited NP-induced cell death. We discovered an interplay between HIF-1α and the autophagy-Zn-reactive oxygen species (ROS)-autophagy cycle axis and revealed that NP-induced cancer cell killing followed a HIF-1α-BNIP3-LC3B-mediated mitophagy pathway. We confirmed that NP-upregulated HIF-1α protein expression was attributed to prolyl hydroxylase inhibition by both ROS and Zn. In addition, the in vivo assay confirmed the therapeutic effectiveness and safety of ZnO NPs on a

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Author

He, Guanping; Pan, Xiaoyu; Liu, Xiao; Zhu, Ye; Ma, Yunlong; Du, Chuanchao; Liu, Xiaoguang; Mao, Chuanbin

Publisher

American Chemical Society; American Chemical Society (ACS) (ISSN 1944-8244)

Published

2020

Language

EN

Field

Engineering (Physical Sciences)