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Naproxen inhibits spontaneous lung adenocarcinoma formation in Kras mice. | LitMetric

Naproxen inhibits spontaneous lung adenocarcinoma formation in Kras mice.

Neoplasia

Center for Cancer Prevention and Drug Development, Hem-Onc, Department of Medicine, Stephenson Cancer Center, University of Oklahoma HSC, Oklahoma City, OK, USA; VA Medical Center, Oklahoma City, OK, USA. Electronic address:

Published: June 2021

AI Article Synopsis

  • Lung cancer is the top cause of cancer-related deaths globally, and this study tested the impact of naproxen (a type of NSAID) on lung adenocarcinoma using a mouse model.
  • Mice genetically prone to lung cancer (Kras mice) that were fed a diet with naproxen showed a significant reduction in the number of lung tumors, particularly adenocarcinomas, compared to those on a control diet.
  • Naproxen decreased inflammation and tumor cell growth, while increasing apoptosis in lung tumors, indicating its potential as a chemoppreventive agent against lung adenocarcinoma.

Article Abstract

Lung cancer is the leading cause of cancer related deaths worldwide. The present study investigated the effects of naproxen (NSAID) on lung adenocarcinoma in spontaneous lung cancer mouse model. Six-week-old transgenic Kras mice (n = 20; male + female) were fed modified AIN-76A diets containing naproxen (0/400 ppm) for 30 wk and euthanized at 36 wk of age. Lungs were evaluated for tumor incidence, multiplicity, and histopathological stage (adenoma and adenocarcinoma). Lung tumors were noticeable as early as 12 wk of age exclusively in the Kras mice. By 36 wk age, 100% of Kras mice on control diet developed lung tumors, mostly adenocarcinomas. Kras mice fed control diet developed 19.8 ± 0.96 (Mean ± SEM) lung tumors (2.5 ± 0.3 adenoma, 17.3 ± 0.7 adenocarcinoma). Administration of naproxen (400 ppm) inhibited lung tumor multiplicity by ∼52% (9.4 ± 0.85; P < 0001) and adenocarcinoma by ∼64% (6.1 ± 0.6; P < 0001), compared with control-diet-fed mice. However, no significant difference was observed in the number of adenomas in either diet, suggesting that naproxen was more effective in inhibiting tumor progression to adenocarcinoma. Biomarker analysis showed significantly reduced inflammation (COX-2, IL-10), reduced tumor cell proliferation (PCNA, cyclin D1), and increased apoptosis (p21, caspase-3) in the lung tumors exposed to naproxen. Decreased serum levels of PGE and CXCR4 were observed in naproxen diet fed Kras mice. Gene expression analysis of tumors revealed a significant increase in cytokine modulated genes (H2-Aa, H2-Ab1, Clu), which known to further modulate the cytokine signaling pathways. Overall, the results suggest a chemopreventive role of naproxen in inhibiting spontaneous lung adenocarcinoma formation in Kras mice.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8187931PMC
http://dx.doi.org/10.1016/j.neo.2021.05.010DOI Listing

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