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- W4366185767 abstract "Oxidative stress has been recognized to be associated with melanoma. We have previously shown that ankyrin repeat-rich membrane spanning (ARMS), a tetra-spanning transmembrane protein, was overexpressed in melanoma cells and conferred resistance to hydrogen peroxide (H2O2)-induced cell death. To explore the molecular mechanism of ARMS in melanoma under oxidative stress, we established ARMS-knockdown (siARMS) melanoma cells and challenged them with H2O2. We found that depletion of ARMS established increased levels of reactive oxygen species (ROS) which contributed to augmented autophagic flux under H2O2 treatment. H2O2-mediated autophagy resulted in non-apoptotic cellular demise in siARMS melanoma cells, as cytoprotective effects were achieved by pretreatment of autophagy inhibitor bafilomycin A1 or by knockdown of autophagy-related 5 (ATG5). Accordingly, reducing ROS by antioxidants in siARMS cells diminished autophagy concomitant with attenuation in cell death. In addition, we found that knockdown of ARMS inhibited H2O2-induced activation of nuclear factor-kappa B signaling pathway and repressed the expression of antioxidant proteins catalase and SOD1 in melanoma cells. Our results suggest silencing ARMS as an alternative therapeutic strategy in treating apoptosis-resistant melanomas by activating ROS-induced autophagy-mediated cell death." @default.
- W4366185767 created "2023-04-19" @default.
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- W4366185767 date "2023-05-01" @default.
- W4366185767 modified "2023-09-28" @default.
- W4366185767 title "1212 Depletion of ARMS in melanoma cells induces autophagy-mediated cell death under oxidative stress" @default.
- W4366185767 doi "https://doi.org/10.1016/j.jid.2023.03.1226" @default.
- W4366185767 hasPublicationYear "2023" @default.
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