Ontology highlight
ABSTRACT:
PROVIDER: PRJNA97195 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression during tumor enhancement by 3,3’-diindolylmethane in rainbow trout: Timecourse
| PRJNA104375 | ENA
Project description:Gene expression during tumor enhancement by 3,3’-diindolylmethane in rainbow trout: HCC tumor samples
| PRJNA104373 | ENA
Project description:Indole-3-carbinol (I3C) and 3,3’-diindolylmethane (DIM), a primary I3C derivative in vivo, are known dietary chemopreventive agents also available as dietary supplements. However, I3C has been found to act as a tumor promoter in rat (multi-organ) and trout (liver) models. I3C and DIM were previously found to be estrogenic in trout liver based on toxicogenomic profiles. In this study, we compare the post-initiation effects of DIM and 17β-estradiol (E2) on aflatoxin B1 (AFB1)-induced hepatocarcinogenesis in trout. Trout were initiated as embryos with 50 ppb AFB1, fed control diet for three months followed by diets containing 0, 120 or 400 ppm DIM or 5 ppm E2 for 18 weeks before returning all groups to control diet. Tumor incidence was determined 13 months later and found to be significantly elevated in AFB1-initiated trout fed either 400 ppm DIM or 5 ppm E2 compared to control animals. To evaluate the mechanism of tumor enhancement, hepatic gene expression profiles were examined in animals fed promotional diets during the course of tumorigenesis and in hepatocellular carcinomas (HCCs) of initiated animals using a rainbow trout 70-mer custom oligonucleotide array. We demonstrate that DIM alters gene expression profiles similar to E2 in liver samples during tumorigenesis and in HCC tumors. Further, HCCs from animals on DIM and E2 promotional diets had a transcriptional signature indicating decreased invasive or metastatic potential compared to HCCs from control animals. Overall, these findings are the first to demonstrate tumor promotion by DIM. They confirm the importance of estrogenic signaling in the mechanism of promotion by dietary indoles in trout liver and indicate a possible dual effect that enhances tumor incidence and decreases potential for metastasis. Keywords: time course
2006-12-31 | GSE5644 | GEO
Project description:Indole-3-carbinol (I3C) and 3,3’-diindolylmethane (DIM), a primary I3C derivative in vivo, are known dietary chemopreventive agents also available as dietary supplements. However, I3C has been found to act as a tumor promoter in rat (multi-organ) and trout (liver) models. I3C and DIM were previously found to be estrogenic in trout liver based on toxicogenomic profiles. In this study, we compare the post-initiation effects of DIM and 17β-estradiol (E2) on aflatoxin B1 (AFB1)-induced hepatocarcinogenesis in trout. Trout were initiated as embryos with 50 ppb AFB1, fed control diet for three months followed by diets containing 0, 120 or 400 ppm DIM or 5 ppm E2 for 18 weeks before returning all groups to control diet. Tumor incidence was determined 13 months later and found to be significantly elevated in AFB1-initiated trout fed either 400 ppm DIM or 5 ppm E2 compared to control animals. To evaluate the mechanism of tumor enhancement, hepatic gene expression profiles were examined in animals fed promotional diets during the course of tumorigenesis and in hepatocellular carcinomas (HCCs) of initiated animals using a rainbow trout 70-mer custom oligonucleotide array. We demonstrate that DIM alters gene expression profiles similar to E2 in liver samples during tumorigenesis and in HCC tumors. Further, HCCs from animals on DIM and E2 promotional diets had a transcriptional signature indicating decreased invasive or metastatic potential compared to HCCs from control animals. Overall, these findings are the first to demonstrate tumor promotion by DIM. They confirm the importance of estrogenic signaling in the mechanism of promotion by dietary indoles in trout liver and indicate a possible dual effect that enhances tumor incidence and decreases potential for metastasis. Keywords: treatment effect
2006-12-31 | GSE5643 | GEO
Project description:Indole-3-carbinol (I3C), from cruciferous vegetables, has been found to suppress or enhance tumors in several animal models. We previously reported that dietary I3C promotes hepatocarcinogenesis in rainbow trout (Oncorhynchus mykiss) at concentrations that differentially activated estrogen receptor (ER) or aryl hydrocarbon receptor (AhR)-mediated responses based on individual protein biomarkers. In this study, we evaluated the relative importance of these pathways as potential mechanisms for I3C on a global scale. Hepatic gene expression profiles were examined in trout after dietary exposure to 500 and 1500 ppm I3C and 3,3,-diindolylmethane (DIM), a major in vivo component of I3C, and were compared to the transcriptional signatures of two model hepatic tumor promoters; 17beta-estradiol (E2), an ER agonist, and beta-naphthoflavone, an AhR agonist. We demonstrate that I3C and DIM acted similar to E2 at the transcriptional level based on correlation analysis of expression profiles and clustering of gene responses. Of the genes regulated by E2 (fold change >2.0 or <0.50), most genes were regulated similarly by DIM (87-92%) and I3C (71%) suggesting a common mechanism of action. Of interest were upregulated genes associated with signaling pathways for cell growth and proliferation, vitellogenesis, and protein folding, stability and transport. Other genes down-regulated by E2, including those involved in acute-phase immune response, were also down-regulated by DIM and I3C. Gene regulation was confirmed by qRT-PCR and western blot. These data indicate I3C promotes hepatocarcinogenesis through estrogenic mechanisms in trout liver and suggest DIM may be an even more potent hepatic tumor promoter in this model. Keywords: dose response
2005-09-28 | GSE3324 | GEO
Project description:Expression profiling of isoflavone and 3,3’-diindolylmethane treated C4-2B prostate cancer cells was conducted using Affymetrix Human Genome U133 Plus 2.0. Array
2012-01-25 | GSE35324 | GEO
Project description:Expression profiling of isoflavone and 3,3’-diindolylmethane treated C4-2B prostate cancer cells was conducted using Affymetrix Human Genome U133 Plus 2.0. Array C4-2B prostate cancer cells were treated with isoflavone and B-DIM for 6 hours or longer up to 72 hours. Gene expression profiling was conducted
2012-01-25 | E-GEOD-35324 | biostudies-arrayexpress
Project description:Effects of sulforaphane and 3,3’-diindolylmethane on genome-wide promoter methylation in normal prostate epithelial cells and prostate cancer cells This study was undertaken to determine the genome-wide effects of sulforaphane (SFN) and 3,3’-diindolylmethane (DIM) on promoter methylation in normal prostate epithelial cells and prostate cancer cells. Nimblegen Human DNA Methylation 3x720K CpG Island Plus RefSeq Promoter Array was used in this study. We hypothesize that both SFN and DIM are effective dietary modulators of DNA methylation due to their inhibitory effects on DNMT expression, and that SFN and DIM can differentially affect the promoter methylation profiles in normal and cancerous prostate epithelial cells.
2014-01-01 | GSE47017 | GEO
Project description:Effects of sulforaphane and 3,3’-diindolylmethane on genome-wide promoter methylation in normal prostate epithelial cells and prostate cancer cells This study was undertaken to determine the genome-wide effects of sulforaphane (SFN) and 3,3’-diindolylmethane (DIM) on promoter methylation in normal prostate epithelial cells and prostate cancer cells. Nimblegen Human DNA Methylation 3x720K CpG Island Plus RefSeq Promoter Array was used in this study. We hypothesize that both SFN and DIM are effective dietary modulators of DNA methylation due to their inhibitory effects on DNMT expression, and that SFN and DIM can differentially affect the promoter methylation profiles in normal and cancerous prostate epithelial cells. Normal prostate epithelial cells (PrEC), androgen-dependent prostate cancer epithelial cells (LnCAP) and androgen-independent prostate cancer epithelial cells (PC3) were treated with vehicle control, 15uM SFN, or 15uM DIM for 48h in triplicates
2014-01-01 | E-GEOD-47017 | biostudies-arrayexpress
Project description:As an important cold-water economic fish species, rainbow trout (Oncorhynchus mykiss) exhibits several intra-specific variation in skin pigmentation that can give rise to distinctive phenotypes, and wild-type rainbow trout with black skin (WR) and yellow mutant rainbow trout with yellow skin (YR) are the major two types in the farms, whose distinct skin colors make them suitable model for elucidating the skin pigmentation process. Skin color as a key indicator for selection in rainbow trout farming as well as has a strong visual impact on the consumer when rainbow trout are marketed. Previously, extensive studies have been conducted on skin color in rainbow trout, including the observation of skin spots and the expression analysis of some important pigment genes. However, up to date, no studies have systematically examined the molecular regulation mechanism of skin color difference between WR and YR through a high throughput method. Therefore, the aim of this study was to reveal the molecular regulation mechanism of skin color difference between these two strains at the mRNA and miRNA transcriptome level, and candidate genes, miRNAs and miRNA-mRNA pairs that may be responsible for rainbow trout albinism were obtained.
2022-04-21 | GSE172482 | GEO