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MeDIP-Chip of PrEC, LnCAP, and PC3 cells treated with vehicle control, sulforaphane, or 3,3’-diindolylmethane

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE47017 | GEO | 2014/01/01

SECONDARY ACCESSION(S): PRJNA203286

REPOSITORIES: GEO

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MeDIP-Chip of PrEC, LnCAP, and PC3 cells treated with vehicle control, sulforaphane, or 3,3’-diindolylmethane

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

global gene expression profiles in primary human hepatocytes exposed to phytochemicals

Project description:Primary human hepatocytes were treated with 2 non-cytotoxic concentrations of sulforaphane (SFN; 10 and 50 uM) phenethyl isothiocyante (PEITC; 10 and 25 uM), 3,3'-diindolylmethane (DIM; 10 and 50 uM), or one concentration of oltipraz (OPZ; 30 uM) for 48 hours. Given the considerable heterogeneity of the human population, it was essential that each experiment was performed with hepatocytes from the same liver, i.e. each liver served as its own control. Each treatment was performed on three batches of human hepatocytes, each derived from a separate liver. 32 arrays, 8 experimental groups.

2010-07-19 | E-GEOD-20479 | biostudies-arrayexpress

global gene expression profiles in primary human hepatocytes exposed to phytochemicals

2010-07-19 | GSE20479 | GEO

Genome-wide analysis of gene expression in isoflavone and 3,3’-diindolylmethane treated C4-2B prostate cancer cells

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

Genome-wide transcriptome analysis of the dietary chemopreventive phytochemical sulforaphane on normal and prostate cancer cells.

Project description:Epidemiological studies provide strong evidence that consumption of cruciferous vegetables, such as broccoli, can significantly reduce the risk of developing cancers. Sulforaphane (SFN), a phytochemical derived from cruciferous vegetables, induces anti-proliferative and pro-apoptotic responses in prostate cancer cells, but not in normal prostate cells. The mechanisms responsible for these specific chemopreventive properties remain unclear. We utilized RNA sequencing to test the hypothesis that SFN modifies the expression of genes that are critical in prostate cancer progression. Normal prostate epithelial cells, and androgen-dependent and androgen-independent prostate cancer cells were treated with 15 µM SFN and the transcriptome was determined at 6 and 24 hour time points. SFN altered the expression of ~3,000 genes in each cell line and the response was highly dynamic over time. SFN influenced the expression of genes in functional groups and pathways that are critical in cancer including cell cycle, apoptosis and angiogenesis, but the specific effects of SFN differed depending on the state of cancer progression. Network analysis suggested that a transcription factor that is overexpressed in many cancers, Specificity protein 1 (Sp1), is a major mediator of SFN-induced changes in gene expression. Nuclear Sp1 protein was significantly decreased by 24 hour SFN treatment in prostate cancer cells, while a related transcription factor, Sp3 protein was only modestly decreased in androgen-independent prostate cancer cells. Overall, the data show that SFN significantly affects gene expression in normal and cancer cells, with key targets in chemopreventive processes, making it a promising dietary anti-cancer agent. Examination of how the transcriptome of normal and prostate cancer cells is altered by treatment with sulforaphane

2014-07-11 | E-GEOD-48812 | biostudies-arrayexpress

Genome-wide analysis of gene expression in isoflavone and 3,3’-diindolylmethane treated C4-2B prostate cancer cells

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

Genome-wide transcriptome analysis of the dietary chemopreventive phytochemical sulforaphane on normal and prostate cancer cells.

2014-07-11 | GSE48812 | GEO

UVB drives transcriptomic and epigenetic reprogramming which can be protected by antioxidant sulforaphane in human skin keratinocytes [RNA-seq]

Project description:Continuous exposure to ultraviolet (UV) is one of the main factors contributing to skin carcinogenesis. Sulforaphane (SFN) is a potent antioxidative agent which has potential to prevent the UV-induced skin cell transformation. We characterized the transcriptome and CpG methylation profile of human keratinocytes (HaCaT cells) treated with UVB and/or SFN using RNA sequencing.

2021-10-07 | GSE185320 | GEO

UVB drives transcriptomic and epigenetic reprogramming which can be protected by antioxidant sulforaphane in human skin keratinocytes [Methyl-seq]

2021-10-07 | GSE185319 | GEO

Gene expression during tumor enhancement by 3,3’-diindolylmethane in rainbow trout: Timecourse

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

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