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10.1016/j.redox.2025.103827 http://scihub22266oqcxt.onion/10.1016/j.redox.2025.103827 40914135!ä!40914135 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=40914135&cmd=llinks): Failed to open stream: HTTP request failed! 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Novel Thioredoxin reductase 1 inhibitor BS1801 relieves treatment resistance and triggers endoplasmic reticulum stress by elevating reactive oxygen species in glioma |pdf=|usr=}}{{40914135}} gab.com Text Novel Thioredoxin reductase 1 inhibitor BS1801 relieves treatment resistance and triggers endoplasmic reticulum stress by elevating reactive oxygen species in glioma JO: Redox Biol http://www.kidney.de/pget.php?&tw=1&pmid=40914135 #FOAvip Glioma patients will inevitably develop resistance to temozolomide (TMZ) leading to tumor recurrence. By comparing genomic differences between primary and recurrent glioma patients, Thioredoxin reductase 1 (TrxR1) was identified as a crucial role in TMZ resistance. Glioma cells elevate the expression level of TXNRD1 to against TMZ-induced reactive oxygen species (ROS), thereby conferring TMZ resistance. BS1801 is a novel small-molecular targeted drug that binds to Cys497/Sec498 activity site of TrxR1, competitively inhibiting its activity. The results showed that glioblastoma cells were time- and dose-dependently inhibited by BS1801 treatment. Additionally, BS1801 treatment elevated ROS levels, resulting in glioblastoma cell cycle arrest, endoplasmic reticulum (ER) stress, mitochondrial dysfunction and apoptosis. Meanwhile, BS1801 synergized with TMZ to significantly inhibit glioblastoma cell proliferation, induce DNA damage and trigger mitochondrial depolarization. The modified BS1801-nano combined with TMZ treatment significantly prolonged the overall survival of intracranial orthotopic glioma mice models. Finally, a predictive model for BS1801 treatment sensitivity was established using patient-derived GBM organoids. In summary, BS1801 treatment can elevate ROS levels, induce glioblastoma cell apoptosis and activate ER stress, thereby relieving TMZ resistance. BS1801 exhibits potent glioma inhibitory effects and potential clinical application. Twit Text FOAVip Novel Thioredoxin reductase 1 inhibitor BS1801 relieves treatment resistance and triggers endoplasmic reticulum stress by elevating reactive oxygen species in glioma ????Redox Biol http://www.kidney.de/pget.php?&tw=1&pmid=40914135 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=40914135 #FOAvip English Wikipedia <ref>{{Cite pmid|40914135}}</ref> Novel Thioredoxin reductase 1 inhibitor BS1801 relieves treatment resistance and triggers endoplasmic reticulum stress by elevating reactive oxygen species in glioma #MMPMID40914135 Chang Y; Chang J; Ji J; Sun J; Hu H; Pang B; Zhang Q; Yin H; Zeng H; Jiang T; Li G; Zeng F Redox Biol 2025[Aug]; 86 (ä): 103827 PMID40914135show ga Glioma patients will inevitably develop resistance to temozolomide (TMZ) leading to tumor recurrence. By comparing genomic differences between primary and recurrent glioma patients, Thioredoxin reductase 1 (TrxR1) was identified as a crucial role in TMZ resistance. Glioma cells elevate the expression level of TXNRD1 to against TMZ-induced reactive oxygen species (ROS), thereby conferring TMZ resistance. BS1801 is a novel small-molecular targeted drug that binds to Cys497/Sec498 activity site of TrxR1, competitively inhibiting its activity. The results showed that glioblastoma cells were time- and dose-dependently inhibited by BS1801 treatment. Additionally, BS1801 treatment elevated ROS levels, resulting in glioblastoma cell cycle arrest, endoplasmic reticulum (ER) stress, mitochondrial dysfunction and apoptosis. Meanwhile, BS1801 synergized with TMZ to significantly inhibit glioblastoma cell proliferation, induce DNA damage and trigger mitochondrial depolarization. The modified BS1801-nano combined with TMZ treatment significantly prolonged the overall survival of intracranial orthotopic glioma mice models. Finally, a predictive model for BS1801 treatment sensitivity was established using patient-derived GBM organoids. In summary, BS1801 treatment can elevate ROS levels, induce glioblastoma cell apoptosis and activate ER stress, thereby relieving TMZ resistance. BS1801 exhibits potent glioma inhibitory effects and potential clinical application. äNovel Thioredoxin reductase 1 inhibitor BS1801 relieves treatment resi(epmc).pdf DeepDyve Pubget Overpricing