NOX1 inhibition attenuates the development of a pro?tumorigenic environment in experimental hepatocellular carcinoma
نویسندگان
چکیده
Abstract Background The poor prognosis of advanced HCC and limited efficacy current systemic treatments emphasize the need for new or combined targeted therapies. development is a multistage process in which liver injury appears complex microenvironment associated with oxidative stress. NOX enzymes are main source ROS during hepatocarcinogenesis NOX1 particular has shown correlation patients. This study evaluates effect pharmacological inhibition on progression its tumor microenvironment. Methods vitro cytotoxic effects inhibitor GKT771 (Genkyotex) human Huh7 Hep3B murine Hepa1-6 cell lines, THP1 monocyte line mouse macrophages were evaluated via MTT, LDH activity CaspGlo® assays. In order to induce vivo HCC, male SV129 wild-type mice received weekly IP injections diethylnitrosamine (DEN) (35 mg/kg) 20–25 weeks. Mice treated vehicle (30 oral gavage, daily twice daily, preventive therapeutic studies. damage was inflammation, angiogenesis, fibrosis histology, RT-qPCR, multiplex analyses levels. Results A concentration-dependent reduction cellular lines without cytotoxicity observed. treatment reduced LPS-induced pro-inflammatory bone-marrow derived macrophage polarization. DEN resulted 100 % formation induction markers could be by dosing at early onset HCC. DEN-induced an upregulation pro-inflammatory, angiogenic fibrotic less pronounced all regimens. line, induced this lesser extend upon treatment. Conclusions showed safe well tolerated able attenuate pro-fibrotic suggesting that might promising adjuvant strategy
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ژورنال
عنوان ژورنال: Journal of Experimental & Clinical Cancer Research
سال: 2021
ISSN: ['1756-9966']
DOI: https://doi.org/10.1186/s13046-021-01837-6