Corrigendum to ‘Butaselen prevents hepatocarcinogenesis and progression through inhibiting thioredoxin reductase activity’ [Redox Biol. 14 (2018) 237–249]
| Autor: | Huihui Zeng, Yuxi Liu, Hanwei Yin, Xiaoqing Zheng, Weiwei Ma, Wei Xu, Ruoxuan Sun, Fei Lin |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
TrxR
thioredoxin reductase Thioredoxin reductase Thioredoxin reductase (TrxR) Clinical Biochemistry Chemoprevention Biochemistry Redox NF-κB ROS reactive oxygen species Trx thioredoxin Hepatocellular carcinoma (HCC) lcsh:QH301-705.5 GPC3 glypican-3 TPA phorbol ester NAC N-acetyl-L-cysteine BS butaselen lcsh:R5-920 Chemistry Organic Chemistry Reactive oxygen species (ROS) lcsh:Biology (General) COX-2 cyclooxygenase-2 IκBs NF-κB inhibitory proteins iNOS inducible nitric oxide synthase SRB sulforhodamine B HCC hepatocellular carcinoma lcsh:Medicine (General) Research Paper DEN diethylnitrosamine |
| Zdroj: | Redox Biology, Vol 32, Iss, Pp-(2020) Redox Biology |
| ISSN: | 2213-2317 |
| Popis: | Hepatocellular carcinoma (HCC) accounts for most of primary liver cancer, of which five-year survival rate remains low and chemoprevention has become a strategy to reduce disease burden of HCC. We aim to explore the in vivo chemopreventive effect of an organoselenium-containing compound butaselen (BS) against hepatocarcinogenesis and its underlying mechanisms. Pre- and sustained BS treatment (9, 18 and 36 mg/Kg BS) could dose-dependently inhibit chronic hepatic inflammation, fibrosis, cirrhosis and HCC on murine models with 24 weeks treatment scheme. The thioredoxin reductase (TrxR), NF-κB pathway and pro-inflammatory factors were activated during hepatocarcinogenesis, while their expression were decreased by BS treatment. BS treatment could also significantly reduce tumor volume in H22-bearing models and remarkably slow tumor growth. HCC cell lines HepG2, Bel7402 and Huh7 were time- and dose-dependently inhibited by BS treatment. G2/M arrest and apoptosis were observed in HepG2 cells after BS treatment, which were mediated by TrxR/Ref-1 and NF-κB pathways inhibition. BS generated reactive oxygen species (ROS), which could be reduced by antioxidant N-acetyl-L-cysteine (NAC) and NADPH oxidase inhibitor DPI. NAC could markedly increase HepG2 cells viability. TrxR activity of HepG2 cells treated with BS were significantly decreased in parallel with proliferative inhibition. The TrxR1-knockdown HepG2 cells also exhibited low TrxR1 activity, high ROS level, relatively low proliferation rate and increased resistance to BS treatment. In conclusion, BS can prevent hepatocarcinogenesis through inhibiting chronic inflammation, cirrhosis and tumor progression. The underlying mechanisms may include TrxR activity inhibition, leading to ROS elevation, G2/M arrest and apoptosis. |
| Databáze: | OpenAIRE |
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