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Arsenic trioxide (As 2 O 3 ) is a promising effective chemotherapeutic agent for cancer treatment; however, how and through what molecular mechanisms the oxidative damage of As 2 O 3  is controlled remains poorly understood. Recently, the involvement of dysregulated long noncoding RNA ovarian tumor domain containing 6B antisense RNA1 (lncRNA OTUD6B-AS1) in tumorigenesis is established. Here, for the first time, we characterize the regulation of As 2 O 3  in the oxidative damage against bladder cancer via lncRNA OTUD6B-AS1. As 2 O 3  could activate lncRNA OTUD6B-AS1 transcription in bladder cancer cells, and these findings were validated in a xenograft tumor model. Functional assays showed that lncRNA OTUD6B-AS1 dramatically exacerbated As 2 O 3 -mediated oxidative damage by inducing oxidative stress. Mechanistically, As 2 O 3  increased levels of metal-regulatory transcription factor 1 (MTF1), which regulates lncRNA OTUD6B-AS1, in response to oxidative stress. Further, lncRNA OTUD6B-AS1 inhibited mitochondrial NADP + -dependent isocitrate dehydrogenase 2 (IDH2) expression by stabilizing miR-6734-5p, which contributed to cytotoxicity by enhancing oxidative stress. Together, our findings offer new insights into the mechanism of As 2 O 3 -induced oxidative damage and identify important factors in the pathway, As 2 O 3 /lncRNA OTUD6B-AS1/miR-6734-5p/IDH2, expanding the knowledge of activity of As 2 O 3  as cancer treatment.

oxidative medicine and cellular longevity

lncRNA OTUD6B-AS1 Exacerbates As<sub>2</sub>O<sub>3</sub>-Induced Oxidative Damage in Bladder Cancer via miR-6734-5p-Mediated Functional Inhibition of IDH2

lncRNA OTUD6B-AS1 Exacerbates As2O3-Induced Oxidative Damage in Bladder Cancer via miR-6734-5p-Mediated Functional Inhibition of IDH2

lncRNA OTUD6B-AS1 Exacerbates As₂O₃-Induced Oxidative Damage in Bladder Cancer via miR-6734-5p-Mediated Functional Inhibition of IDH2