Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cancer prevention by phenethyl isothiocyanate (PEITC) in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice [methyl-Seq]

ABSTRACT: The glucosinolate-derived phenethyl isothiocyanate (PEITC) has been widely reported to reduce the risk of prostate cancer by modulating multiple biologically relevant activities. Emerging evidence suggests that PEITC may exert its anti-cancer effects through epigenetic mechanisms including alterations of DNA methylation. The purpose of this study was to examine the effects of PEITC on prostate carcinogenesis in a murine prostate cancer model (TRAMP). 8 weeks old TRAMP males were fed AIN-93M control diet or diet containing 0.05% PEITC for 8 or16 weeks. We observed reduced tumor incidence in PEITC group (0/5) at 24 weeks of age as compared to control diet group (6/7). We also performed Next-generation sequencing (RNA-seq and SureSelect Methyl-seq) with non-tumor and tumor prostate tissue collected from the above-mentioned TRAMP groups and time matching wildtype (not TRAMP) control diet groups at the same time points. Our bioinformatic analyses reveal that several carcinogenesis pathways as well as pathways of inflammation and cell proliferation were activated in TRAMP group as compared to wildtype group. Surprisingly, these pathways were inhibited by PEITC diet administration. We also identified a number of genes with inverse regulation relationship between their RNA expression and their CpG methylation during prostate carcinogenesis and cancer prevention by PEITC in TRAMP mice. Our study demonstrated that PEITC administration can suppress prostate cancer by epigenetic regulation of key genes. [This GEO/dataset is the bisulfite methyl-seq part of the study.]

ORGANISM(S): Mus musculus

PROVIDER: GSE140311 | GEO | 2023/01/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Cancer prevention by phenethyl isothiocyanate (PEITC) in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice [RNA-Seq]

Project description:The glucosinolate-derived phenethyl isothiocyanate (PEITC) has been widely reported to reduce the risk of prostate cancer by modulating multiple biologically relevant activities. Emerging evidence suggests that PEITC may exert its anti-cancer effects through epigenetic mechanisms including alterations of DNA methylation. The purpose of this study was to examine the effects of PEITC on prostate carcinogenesis in a murine prostate cancer model (TRAMP). 8 weeks old TRAMP males were fed AIN-93M control diet or diet containing 0.05% PEITC for 8 or16 weeks. We observed reduced tumor incidence in PEITC group (0/5) at 24 weeks of age as compared to control diet group (6/7). We also performed Next-generation sequencing (RNA-seq and SureSelect Methyl-seq) with non-tumor and tumor prostate tissue collected from the above-mentioned TRAMP groups and time matching wildtype (not TRAMP) control diet groups at the same time points. Our bioinformatic analyses reveal that several carcinogenesis pathways as well as pathways of inflammation and cell proliferation were activated in TRAMP group as compared to wildtype group. Surprisingly, these pathways were inhibited by PEITC diet administration. We also identified a number of genes with inverse regulation relationship between their RNA expression and their CpG methylation during prostate carcinogenesis and cancer prevention by PEITC in TRAMP mice. Our study demonstrated that PEITC administration can suppress prostate cancer by epigenetic regulation of key genes. [This GEO/dataset is the RNA-seq part of the study.]

2023-01-01 | GSE140310 | GEO

Cancer prevention by phenethyl isothiocyanate (PEITC) in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice [methyl-Seq]

Project description:Cancer prevention by phenethyl isothiocyanate (PEITC) in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice [methyl-Seq]

| PRJNA589284 | ENA

High Fat Diet Reduces the Expression of Glutathione Peroxidase 3 in Mouse Prostate

Project description:High fat diets are known to be a risk factor for prostate cancer. In this study, we investigated the effect of high fat diet on mouse prostate gene expression. C57BL/6J mice were fed either a control or high fat diet for 12 weeks. Microarray analyses were performed on mouse ventral prostate (VP) and dorsolateral prostate (DLP), followed by canonical pathway analysis and regulatory network identification. mRNA changes were confirmed by real time PCR. Approximately 2,125, and 1,194 genes responded significantly to the high fat diet in VP, DLP, respectively. Pathways and networks related to oxidative stress, glutathione metabolism, NRF-mediated oxidative stress response and NF-kappaB were all differentially regulated by high fat diet. GPx3 mRNA levels were decreased by approximately 2-fold by high fat diet in all 3 prostate lobes. In human non-transformed prostate cells (PrSC, PrEC and BPH-1), cholesterol loading decreased GPx3 expression, and increased H2O2 levels of culture medium. Troglitazone increased GPx3 expression in 3 normal prostate cells, and decreased H2O2 levels. In addition, troglitazone attenuated cholesterol-induced H2O2 increase. Tissue from prostate cancer biopsies had decreased GPx3 mRNA and its level was inversely related to the Gleason score. High fat diet alters pathways related to many genes concerned with oxidative stress. GPx3, a gene identified by this analysis, was found to be down regulated by high fat diet and appears be decreased in human prostate cancers, suggesting that GPx3 may have a possible role in modulating carcinogenesis. Control group:5 C57BL/6J mice (Taconic, Hudson, NY), 8-weeks of age, fed control diet ad libitum for 12 weeks; Experimental group: 5 C57BL/6J mice (Taconic, Hudson, NY), 8-weeks of age, fed ad libitum high fat diet for 12 weeks.

2012-01-02 | E-GEOD-26464 | biostudies-arrayexpress

Hsa-miR-1-2/miR-133a-1 cluster expression silencing by DNA hypermethylation triggers oncogenes contributing to prostate cancer aggressiveness

Project description:We developed a metabolic syndrome (MeS)-like disease model using C57BL/6J mice chronically fed with high fat diet (HFD) that were inoculated with TRAMP-C1 prostate cancer (PCa) cells to investigate the effect of a HFD on the expression of cancer-related miRNAs. In this dataset, we include the expression data obtained from TRAMP-C1 tumors developed in control diet (CD) versus high fat diet (HFD) C57BL/6J male mice. For differential expression analysis we used the Rank Product Method for two class unpaired data and a fold discovery rate (FDR) < 0.05 .

2022-11-16 | GSE181350 | GEO

The Aged Microenvironment Enhances the Tumorigenic Potential of Malignant Prostate Epithelial Cells

Project description:The incidence of prostate cancer is directly linked to age, but we still lack an adequate understanding of the prostatic aging-associated changes that facilitate carcinogenesis. In this study, we investigated possible associated factors in the aged prostate microenvironment, using an orthotopic mouse model of prostate cancer. We found that aged mice showed accelerated growth of TRAMP-C2 cells, compared with young mice. Metastatic lesions following intravenous injection were also more numerous in aged mice. TRAMP-C2 tumors from young and aged mice showed no significant differences concerning their proliferation index, apoptosis or angiogenesis. However, analysis of tumor-infiltrating immune cells by immunohistochemistry and RNA-seq gene expression revealed that aged mice present higher numbers of macrophages in normal prostatic tissue and that these are quickly polarized towards an M2 phenotype upon TRAMP-C2 cells engraftment.

2019-04-23 | GSE110643 | GEO

Gene expression profile of Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP)

Project description:Gene expression profile of Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) reveals murine targets for preclinical development of human prostate cancer therapy In this study, we have generated an open source TRAMP microarray dataset to identify differentially expressed genes from human prostate cancer that have concordant expression in TRAMP tumors, and thereby represent lead targets for preclinical therapy development. Affymetrix Mouse 430 2.0 chips were used for microarrays of total RNA from 9 TRAMP tumors and 9 normal prostates (ventral and dorsolateral lobes). Keywords: prostate cancer, TRAMP

2008-12-31 | GSE10525 | GEO

Genetic deletion of osteopontin in TRAMP mice enhances the growth of aggressive prostate cancer with feature of human neuroendocrine tumors

Project description:Osteopontin (OPN) is a secreted glycoprotein, belonging to the non-structural extracellular matrix (ECM), and its over expression in human prostate cancer cells has been associated with disease progression, androgen independence and metastases. Nevertheless the pathophysiology of OPN in prostate tumorigenesis has never been studied. We crossed TRansgenic Adenocarcinoma of the Mouse Prostate (TRAMP) mice with OPN deficient (OPN-/-) mice and followed tumor onset and progression in these double mutants. Ultrasound examination detected the early onset of a spherical homogeneous tumor in about 60% of OPN-/- TRAMP mice that seldom occurs in parental TRAMP mice. Histology and immunohistochemistry characterized these tumors for being Tag positive but negative for AR, highly proliferative and endowed of neuroendocrine (NE) features. Gene expression profiling showed up-regulation of genes involved in tumor progression, cell cycle and neuronal differentiation in OPN-deficient versus -sufficient TRAMP tumors. Down-regulated genes included key genes of TGFï?¢ pathway, and a role for TGFï?¢ in NE differentiation of prostate cancer was also confirmed at the protein level. Furthermore, NE genes and particularly those characterizing early prostatic lesions of OPN-deficient mice were found to correlate with those of human NE tumours. These data underscore a novel role of OPN at early stages of prostate cancer growth, protecting against the development of aggressive NE tumors. Total RNA obtained from prostate tumors from 18 and 30 weeks old TRAMP mice, compared to RNA extracted from prostate tumors and prostate tissue from Osteopontin-deleted TRAMP mice

2016-01-20 | E-GEOD-69903 | biostudies-arrayexpress

Cancer prevention by phenethyl isothiocyanate (PEITC) in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice

Project description:Cancer prevention by phenethyl isothiocyanate (PEITC) in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice

| PRJNA589278 | ENA

Sox9 mediated differential gene expression was assessed in prostaspheres derived from urogenital sinus epithelial cells

Project description:Prostate cancer is one of the most common malignancies and the second leading cause of death from cancer in men. The molecular mechanisms driving prostate carcinogenesis are complex; with several lines of evidence suggesting that the re-expression of conserved developmental programs play a key role. Through conditional gene targeting and organ grafting, we describe conserved roles for the transcription factor Sox9 in the initiation of both prostate organogenesis and prostate carcinogenesis in murine models. Abrogation of Sox9 expression prior to the initiation of androgen signaling blocks the initiation of prostate development. Similarly, Sox9 deletion in two genetic models of prostate cancer (TRAMP and Hi-Myc) blocks cancer initiation. Expression profiling of Sox9-null prostate epithelial cells reveals that the role of Sox9 in the initiation of prostate development may relate to its regulation of multiple cytokeratins and/or calcium-related proteins. Due to its essential role in cancer initiation, manipulation of Sox9 targets in at-risk men may prove useful in the chemoprevention of prostate cancer.

2013-01-01 | GSE35419 | GEO

Adipose tissue from metabolic syndrome mice induces an aberrant miRNA signature highly relevant in prostate cancer development

Project description:We developed a MeS-like disease model using C57BL/6J mice chronically fed with high fat diet (HFD) that were inoculated with TRAMP-C1 prostate cancer (PCa) cells to investigate the interaction between white adipose tissue (WAT) and PCa cells through miRNAs, in MeS mice. In this dataset, we include the expression data obtained from co-culture medium between TRAMP-C1 cells with HFD-gonadal WAT (gWAT) versus TRAMP-C1 cells with CD-gWAT. For differential expression analysis we used the Rank Product Method.

2020-11-09 | GSE149506 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data