The compound 2‐(naphthalene‐2‐thio)‐5,8‐dimethoxy‐1,4‐naphthoquinone induces apoptosis via reactive oxygen species‐regulated mitogen‐activated protein kinase, protein kinase B, and signal transducer and activator of transcription 3 signaling in human gastric cancer cells

摘要: Hit, Lead & Candidate Discovery It is reported that 1,4-naphthoquinones and their derivatives have potent antitumor activity in various cancers, although clinical application limited by observed side effects. To improve the therapeutic efficacy of naphthoquinones treatment cancer to reduce effects, we synthesized a novel naphthoquinone derivative, 2-(naphthalene-2-thio)-5,8-dimethoxy-1,4-naphthoquinone (NTDMNQ). In this study, explored effects NTDMNQ on apoptosis gastric cells with focus reactive oxygen species (ROS) production. Our results demonstrated exhibited cytotoxic dose-dependent manner. significantly induced mitochondrial-related AGS increased accumulation ROS. However, pre-treatment N-acetyl-L-cysteine (NAC), an ROS scavenger, inhibited NTDMNQ-induced apoptosis. addition, phosphorylation p38 kinase c-Jun N-terminal (JNK) decreased extracellular signal-regulated (ERK), protein B (Akt), Signal Transducer Activator Transcription 3 (STAT3); these were blocked mitogen-activated (MAPK) inhibitor NAC. Taken together, present findings indicate cell via ROS-mediated regulation MAPK, Akt, STAT3 signaling pathways. Therefore, may be potential for as well other tumor types.