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Transcriptomic profile in the liver of rats treated with the chemopreventive butyrate-containing structured lipids.

ABSTRACT: It is widely believed that the prevention of cancer is the most promising strategy for reducing both cancer incidence and cancer-related mortality. Dietary bioactive components have been found to modulate many dysregulated molecular pathways associated with the development of cancer. Epidemiological and pre-clinical data suggest that sodium butyrate and its derivatives possess chemopreventive properties. Specifically, the butyrate-containing structured lipid (STL) presented strong chemopreventive proprieties in experimental hepatocarcinogenesis. To determine the mechanistic basis, the hepatic transcriptomic profiles in rats submitted to a classic “resistant hepatocyte” model of hepatocarcinogenesis and treated with butyrate-containing STL were evaluated. A total of 1583 genes were found to be differentially expressed in the livers of rats treated with butyrate-containing STL. Pathways analysis of the differentially expressed genes demonstrated a strong enrichment in genes involved in epithelial mesenchymal transition, vasculogenesis, and cell proliferation. In conclusion, tumor-suppressing activity of butyrate containing STLs is associated with its ability to regulated major hepatocarcinogenesis-related pathways at early stages of rat liver carcinogenesis.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE109685 | GEO | 2018/01/26

REPOSITORIES: GEO

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Project description:Purpose: Chronic pulmonary inflammation in the form of chronic obstructive pulmonary disease (COPD) has been consistently shown to increase the risk of lung cancer. Therefore, identification of chemopreventive agents with anti-inflammatory effects, in addition to antiproliferative and apoptotic activities, is indispensable. Recently, we found that combinations of silibinin (Sil) and indole-3-carbinol (I3C) significantly inhibited lung tumorigenesis induced by 4-(methylnitro-samino)-1-(3-pyridyl)-1-butanone (NNK) and enhanced by chronic treatment with the inflammatory agent lipopolysaccharide (LPS). In this study, we described gene expression profiling of lung tissues using RNA-seq to determine the gene expression signature in inflammation-driven lung tumors and modulation of this signature by the chemopreventive agents Sil and I3C. Methods: Total RNA extracted from lung tissues of control and treated mice were processed for mRNA sequencing, in triplicate, using Illumina HiSeq 2000. The sequence reads that passed quality filters were analyzed for transcript abundance at the gene level using CLC Bio Genomics Workbench and differential gene expression analysis was performed using the built-in Empirical Analysis of Differential Gene Expression (DGE) based on 'Exact Test' method. qRTâPCR validation was performed using SYBR Green assays. Results and conclusions: We found that 330, 2,957, and 1,143 genes were differentially regulated in mice treated with NNK, LPS, and NNK + LPS, respectively. The expression of inflammation-and immunity-related genes was significantly more deregulated in lung tissues of mice treated with LPS alone compared to mice treated with NNK + LPS. Among 1,143 genes differentially regulated in the NNK + LPS group, the expression of 162 genes and associated signaling pathways were significantly modulated by I3C and/or Sil + I3C. These genes include cytokines, chemokines, and genes with a well-established role in inflammation and/or tumorigenesis such as c-ros oncogene 1 (Ros1), the EGFR ligands amphiregulin and epiregulin, Cyp1a1, and the circadian rhythm genes Arntl, and Npas2. To 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. Lung tissue mRNA profiles of mice treated with control vehicle, NNK, LPS, NNK+LPS, or NNK+LPS supplemented with chemopreventive agent(s) were generated by deep sequencing, in triplicate, using Illumina HiSeq 2000.

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Transcriptomic profile in the liver of rats treated with the chemopreventive butyrate-containing structured lipids.

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