MicroRNA expression in lung tumors of viny-carbamate treated and viny-carbamate and indole-3-carbinol treated mice
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ABSTRACT:
ORGANISM(S): Mus musculus Danio rerio Rattus norvegicus Homo sapiens Caenorhabditis elegans Drosophila melanogaster
PROVIDER: GSE16490 | GEO | 2009/12/06
SECONDARY ACCESSION(S): PRJNA116007
REPOSITORIES: GEO
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Project description:We examined the differential expression of miRNAs in vinyl carbamate (VC)-induced lung tumors in A/J mice and assessed if the chemopreventive agent indole-3-carbinol (I3C) reversed the effects of the carcinogen. Microarray studies revealed some up-regulated microRNAs, but down-regulation of several microRNAs in carcinogen-treated mice relative to vehicle-treated mice. Keywords: Expression micro and control RNA from control treated (3 replicates), vinyl carbamate treated (4 replicates) and vinyl carbamate and indole-3-carbinol treated mice was hybridized versus synthetic human DNA to a custom multi-organism oligonucleotide array.
2010-05-18 | E-GEOD-16490 | biostudies-arrayexpress
Project description:Indole-3-carbinol (I3C) is a natural anti-carcinogenic compound found at high concentrations in Brassica vegetables. ER-positive cell lines demonstrated the greatest sensitivity to the anti-tumor effects of I3C compared to ER-negative breast cancer cell lines. Gene expression analysis was performed to identify genes and pathways that accounted for sensitivity to I3C. Microarray analysis performed using Illumina HT-12 v4 expression arrays
2014-08-12 | GSE55897 | GEO
Project description:Indole-3-carbinol (I3C) is a natural anti-carcinogenic compound found at high concentrations in Brassica vegetables. ER-positive cell lines demonstrated the greatest sensitivity to the anti-tumor effects of I3C compared to ER-negative breast cancer cell lines. Gene expression analysis was performed to identify genes and pathways that accounted for sensitivity to I3C. Microarray analysis performed using Illumina HT-12 v4 expression arrays A total of 36 samples were analyzed with six breast cancer cell lines treated with either the vehicle control or the drug Indole-3-carbinol in triplicate. The cell lines were: MCF-7, T47D, ZR751(sensitive to the drug, apoptosis/growth arrest) and MDA-MB-231, MDA-MB-157, and MDA-MB-436 (insensitive to the drug). Sensitive cell lines are of the luminal subtype and insensitive cell lines are of the basal subtype.
2014-08-12 | E-GEOD-55897 | biostudies-arrayexpress
Project description:Rodent studies have indicated that gestational and perinatal bisphenol A (BPA) exposure increase the risk of developing breast cancer during adulthood. In contrast, some dietary compounds such as genistein (GEN) and indole 3-carbinol (I3C) present potential protective effects against inducing hormone-dependent cancers, including that of the mammary gland. Thus, we aimed to evaluate the role of these dietary compounds on early mammary gland development and carcinogenesis in female Sprague-Dawley offspring. Pregnant Sprague-Dawley (SD) rats were treated with BPA at 25 or 250µg/kg b.w./day by gavage from gestational day (GD) 10 to 21 with or without dietary GEN (250 mg/kg chow, ~5.5 mg/kg b.w./day) or I3C (2000 mg/kg chow, ~45.0 mg/kg b.w./day). At post-natal day (PND) 21, some female offspring from different litters were euthanized for mammary gland development and gene expression analyses while other female offspring received a single dose of N-methyl-N-nitrosourea (MNU) for mammary carcinogenesis initiation. The findings this study indicated the prenatal exposure to BPA, GEN and I3C did not significantly alter ductal elongation, number of terminal end buds (TEB) or cell proliferation, and estrogen receptor alpha (ER-α) immunostaining expression in epithelial mammary cells at PND 21. BPA treatment modulated the expression of several genes, but these changes were not associated with a dose dependent response. Dietary GEN and I3C treatment causally and consistent with the mammary gland structures outcomes. Besides, maternal BPA exposure associated with dietary GEN and I3C did not alter the susceptibility to the mammary cancer development in adulthood when the carcinogen was administered in a window of immature mammary gland development.
2016-06-03 | GSE68973 | GEO
Project description:We previously showed that exposure of rats to environmental cigarette smoke (ECS) causes extensive downregulation of microRNA expression in the lung, resulting in overexpression of multiple genes and proteins. In the present study, we evaluated by microarray the expression of 484 microRNAs in the lung of rats receiving orally chemopreventive agents, including N-acetylcysteine, oltipraz, indole-3-carbinol, 5,6-benzoflavone and phenethyl isothiocyanate, or combinations thereof. Scatterplot, hierarchical cluster, and principal component analyses showed that none of the above chemopreventive regimens appreciably affected the baseline microRNA expression, while all of them attenuated ECS-induced alterations but to a variable extent. Thus, mirnome analysis provides a new tool for predicting both safety and efficacy of cancer chemopreventive agents at early carcinogenesis stages. Keywords: cancer chemoprevention, microRNA, environmental cigarete smoke (ECS), 5,6-benzoflavone (BF), Indole 3-carbinol (I3C),N-acetylcysteine (NAC), oltipraz (OPZ), Phenethyl isothiocyanate (PEITC).
2009-12-21 | GSE19540 | GEO
Project description:Necrotizing enterocolitis (NEC) causes significant morbidity and mortality in premature infants; therefore, the identification of therapeutic and preventative strategies against NEC remains a high priority. The ligand-dependent transcription factor aryl hydrocarbon receptor (AhR) is well known to contribute to the regulation of intestinal microbial communities and amelioration of intestinal inflammation. However, the role of AhR signaling in NEC is unclear. Experimental NEC was induced in four-day-old wild-type mice or mice lacking AhR expression in the intestinal epithelial cells (AhRΔrIEC) or in CD11c+ cells (AhRΔrCD11c) by subjecting animals to twice daily hypoxic stress and gavage feeding with formula supplemented with lipopolysaccharide and enteric bacteria. During NEC, compared to wild-type mice treated with vehicle, littermates treated with an AhR pro-ligand, indole-3-carbinol (I3C), had reduced expression of Il1b and Marco, a scavenger receptor that mediates dendritic cell activation and the recognition and clearance of bacterial pathogens by macrophages. Furthermore, I3C treatment lead to the downregulation of genes involved in cytokine and chemokine as revealed by pathway enrichment analysis. AhRΔrIEC and their cre-negative mouse littermates were similarly susceptible to experimental NEC, whereas AhRΔrCD11c mice with NEC exhibited heightened inflammatory responses compared to their cre-negative mouse littermates. In seeking to determine the mechanisms involved in this increased inflammatory response, we identified the Tim-4- monocyte-dependent subset of macrophages as increased in AhRΔrCD11c mice compared to their cre-negative littermates. Taken together, these findings demonstrate the potential for AhR ligands as a novel immunotherapeutic approach to the management of this devastating disease.
2021-03-03 | GSE154617 | GEO
Project description:We previously showed that exposure of rats to environmental cigarette smoke (ECS) causes extensive downregulation of microRNA expression in the lung, resulting in overexpression of multiple genes and proteins. In the present study, we evaluated by microarray the expression of 484 microRNAs in the lung of rats receiving orally chemopreventive agents, including N-acetylcysteine, oltipraz, indole-3-carbinol, 5,6-benzoflavone and phenethyl isothiocyanate, or combinations thereof. Scatterplot, hierarchical cluster, and principal component analyses showed that none of the above chemopreventive regimens appreciably affected the baseline microRNA expression, while all of them attenuated ECS-induced alterations but to a variable extent. Thus, mirnome analysis provides a new tool for predicting both safety and efficacy of cancer chemopreventive agents at early carcinogenesis stages. Keywords: cancer chemoprevention, microRNA, environmental cigarete smoke (ECS), 5,6-benzoflavone (BF), Indole 3-carbinol (I3C),N-acetylcysteine (NAC), oltipraz (OPZ), Phenethyl isothiocyanate (PEITC). Adult male Sprague-Dawley rats (Harlan Italy, Correzzana, Milan, Italy), weighing 315-320 g, were divided into 16 groups, each composed of 8 animals. Half of them were exposed to ECS for 28 consecutive days, as previously described (Izzotti et al., 2005), while the remaining rats (Sham-exposed) were kept for the same period of time in filtered air. The rats belonging to 14 groups were treated with chemopreventive agents, starting 3 days before exposure to ECS.
2010-05-16 | E-GEOD-19540 | biostudies-arrayexpress
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.
2016-07-03 | E-GEOD-64027 | biostudies-arrayexpress
Project description:Indole-3-carbinol is used as a dietary supplement and has potential use as a therapeutic agent for the prevention of various types of cancer. While substantial evidence exists that indole-3-carbinol can reduce the risk of cancers induced by several known carcinogens when administered to animals, indole-3-carbinol can also function as an initiator and tumor promoter in certain models. The carcinogenic potential of indole-3-carbinol has not been studied in a 2-year bioassay. The objective of the microarray study was to evaluate the transcriptional changes in liver from rats exposed to 0 or 300 mg/kg indole-3-carbinol. At 3 months, livers were analyzed from female Harlan Sprague Dawley rats in the 2-year gavage study of indole-3-carbinol.
2014-07-17 | GSE59287 | GEO
Project description:Indole-3-carbinol is used as a dietary supplement and has potential use as a therapeutic agent for the prevention of various types of cancer. While substantial evidence exists that indole-3-carbinol can reduce the risk of cancers induced by several known carcinogens when administered to animals, indole-3-carbinol can also function as an initiator and tumor promoter in certain models. The carcinogenic potential of indole-3-carbinol has not been studied in a 2-year bioassay. The objective of the microarray study was to evaluate the transcriptional changes in liver from rats exposed to 0 or 300 mg/kg indole-3-carbinol. At 3 months, livers were analyzed from female Harlan Sprague Dawley rats in the 2-year gavage study of indole-3-carbinol. Female rats were administered 300 mg indole-3-carbinol/kg body weight in corn oil by gavage, 5 days per week in a 2 year toxicology study of indole-3-carbinol. Gene expression studies were performed on rat liver with samples hybridized to whole rat genome RG230_2.0 rat GeneChip arrays (Affymetrix, CA).
2014-07-17 | E-GEOD-59287 | biostudies-arrayexpress