ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2015
RNA-sequencing studies identify genes differentially regulated during inflammation-driven lung tumorigenesis and targeted by chemopreventive agents.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 12 citations in OpenAlex.
- Multi-Omics Analysis of the Epigenetic Effects of Inflammation in Murine Type II Pneumocytes.International journal of molecular sciences · 2025Article
- A Multi-Omics Study of Epigenetic Changes in Type II Alveolar Cells of A/J Mice Exposed to Environmental Tobacco Smoke.International journal of molecular sciences · 2024Article
- Genomically Complex Human Angiosarcoma and Canine Hemangiosarcoma Establish Convergent Angiogenic Transcriptional Programs Driven by Novel Gene Fusions.Molecular cancer research : MCR · 2021Article
- Lipopolysaccharide-Mediated Chronic Inflammation Promotes Tobacco Carcinogen-Induced Lung Cancer and Determines the Efficacy of Immunotherapy.Cancer research · 2021Article
- Epigenetic Changes in Alveolar Type II Lung Cells of A/J Mice Following Intranasal Treatment with Lipopolysaccharide.Chemical research in toxicology · 2019Article
- [Study on Effects and Mechanisms of Phytochemicals in Vegetables and Fruits in Preventing and Treating Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2017Review
- Transcriptome profiling in oral cavity and esophagus tissues from (S)-N'-nitrosonornicotine-treated rats reveals candidate genes involved in human oral cavity and esophageal carcinogenesis.Molecular carcinogenesis · 2016Article
- Advances in the Study of Circadian Genes in Non-Small Cell Lung Cancer.Integrative cancer therapiesArticle
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7 authors at 1 institution in 1 country.
Funding
Abstract
introductionChronic pulmonary inflammation has been consistently shown to increase the risk of lung cancer. Therefore, assessing the molecular links between the two diseases and identification of chemopreventive agents that inhibit inflammation-driven lung tumorigenesis is indispensable. MATERIALS AND
methodsFemale A/J mice were treated with the tobacco smoke carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and lipopolysaccharide (LPS), a potent inflammatory agent and constituent of tobacco smoke, and maintained on control diet or diet supplemented with the chemopreventive agents indole-3-carbinol (I3C) and/or silibinin (Sil). At the end of the study, mice were sacrificed and tumors on the surface of the lung were counted and gene expression levels in lung tissues were determined by RNA sequencing.
resultsThe mean number of lung tumors induced by NNK and NNK + LPS was 5 and 15 tumors/mouse, respectively. Dietary supplementation with the combination of I3C and Sil significantly reduced the size and multiplicity (by 50 %) of NNK + LPS-induced lung tumors. Also, we found that 330, 2957, and 1143 genes were differentially regulated in mice treated with NNK, LPS, and NNK + LPS, respectively. The inflammatory response of lung tumors to LPS, as determined by the number of proinflammatory genes with altered gene expression or the level of alteration, was markedly less than that of normal lungs. Among 1143 genes differentially regulated in the NNK + LPS group, the expression of 162 genes and associated signaling pathways was significantly modulated by I3C and/or Sil + I3C. These genes include cytokines, chemokines, putative oncogenes and tumor suppressor genes and Ros1, AREG, EREG, Cyp1a1, Arntl, and Npas2.
conclusionTo our knowledge, this is the first report that provides insight into genes that are differentially expressed during inflammation-driven lung tumorigenesis and the modulation of these genes by chemopreventive agents.
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