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• W4285394037 abstract "Abstract Background Lung cancer has risen to the top of the list of cancer‐related deaths worldwide. Aliskiren is a direct renin inhibitor. Aim This study aims to investigate the impact of cell signaling of Renin‐Angiotensin system (RAS)/NF‐κB on lung cancer by investigating the potential therapeutic effects of aliskiren for lung cancer treatment in urethane‐induced lung cancer in mice. Methods Male BALB/c mice were randomly assigned to one of five treatment groups for 150 days, including (1) normal control; (2) aliskiren (25 mg/kg/i.p) daily, (3) urethane at a dose of 1.5 g/kg (i.p) at Day 1 and 60 (nonsmall cell lung cancer[NSCLC] group) (4) NSCLC mice received carboplatin (15 mg/kg/i.p) every other day for the last 4 successive weeks and (5) NSCLC mice treated with aliskiren daily. Tumor size was determined based on blood sampling, and lungs were isolated for biochemical analysis, western blot analysis assay, and histopathological examination. Results Urethane demonstrated significant changes in all biochemical and molecular parameters and histological patterns. Aliskiren‐treated mice had significantly lower levels of NF‐κB p65, Bcl‐2, cyclin D1, ICAM‐1, MMP‐2, and Nrf2, with an increase in the catalytic activity of caspase‐3 due to its RAS inhibitory mechanism. The combined urethane administration with aliskiren demonstrated a significant improvement in the histopathological examination. Conclusion RAS/NF‐B cell signaling is a potential therapeutic target for preventing and treating lung adenocarcinoma, evidenced by the fundamental cytotoxic mechanism and attenuation of metastasis and angiogenesis induced by the treatment of NSCLC mice with aliskiren." @default.
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• W4285394037 date "2022-07-13" @default.
• W4285394037 modified "2023-10-01" @default.
• W4285394037 title "Novel therapeutic modalities target cell signaling of Renin‐Angiotensin system/NF‐κB‐induced cell cycle arrest and apoptosis in urethane‐induced lung cancer in mice: An in vivo study" @default.
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• W4285394037 doi "https://doi.org/10.1002/jbt.23162" @default.
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