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

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

PROVIDER: PRJNA589284 | ENA |

REPOSITORIES: ENA

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Cancer prevention by phenethyl isothiocyanate (PEITC) in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice [methyl-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 bisulfite methyl-seq part of the study.]

2023-01-01 | GSE140311 | GEO

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

2023-01-01 | GSE140310 | GEO

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

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

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

| PRJNA589285 | ENA

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-01-01 | GSE140314 | GEO

Substrate Specificity of the TRAMP Nuclear Surveillance Complexes

Project description:During nuclear surveillance in yeast, the RNA exosome functions together with the TRAMP complexes. These include the DEAH-box RNA helicase Mtr4 together with an RNA-binding protein (Air1 or Air2) and a poly(A) polymerase (Trf4 or Trf5). To better determine how RNA substrates are targeted, we analyzed protein and RNA interactions for TRAMP components. Mass spectrometry identified three distinct TRAMP complexes formed in vivo. These complexes preferentially assemble on different classes of transcripts. Unexpectedly, on many substrates, including pre-rRNAs and pre-mRNAs, binding specificity was apparently conferred by Trf4 and Trf5. Clustering of mRNAs by TRAMP association showed coenrichment for mRNAs with functionally related products, supporting the significance of surveillance in regulating gene expression. We compared binding sites of TRAMP components with multiple nuclear RNA binding proteins, revealing preferential colocalization of subsets of factors. TRF5 deletion reduced Mtr4 recruitment and increased RNA abundance for mRNAs specifically showing high Trf5 binding.

2020-07-02 | PXD017114 | Pride

Expression data derived from adenocarcinoma or neuroendocrine prostate cancer of TRAMP and SPARC deficient TRAMP mice.

Project description:In this dataset we show transcriptional profiles derived from adenocarcinoma or incipient neuroendocrine prostate cancer (NEPC) derived from TRAMP or SPARC-deficient TRAMP mice respectively. Genetic ablation of SPARC rendered prostate cancer cells to be prone to NEPC differentiation.

2024-07-01 | GSE242811 | GEO

Gene expression profiling of caffeic acid phenethyl ester -treated human umbilical vein endothelial cells

Project description:This SuperSeries is composed of the following subset Series: GSE10413: Gene expression profiling of caffeic acid phenethyl ester-treated human umbilical vein endothelial cells-1 GSE10429: Gene expression profiling of caffeic acid phenethyl ester -treated human umbilical vein endothelial cells-2 Keywords: SuperSeries Refer to individual Series

2010-05-26 | E-GEOD-10465 | biostudies-arrayexpress

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

Tumor regression by phenethyl isothiocyanate involves DDB2.

Project description:Phenethyl isothiocyanate (PEITC) is a promising cancer chemopreventive agent commonly found in edible cruciferous vegetables. It has been implicated also for therapy, and is in clinical trial for lung cancer. Here, we provide evidence that the tumor suppressive effect of PEITC is related to its ability to induce expression of damaged DNA binding protein 2 (DDB2), a DNA repair protein involved also in apoptosis and premature senescence. DDB2 expression is attenuated in a wide variety of cancers including the aggressive colon cancers. We show that, in colon cancer cells, reactive oxygen species, which are induced by PEITC, augment expression of DDB2 through the p38MAPK/JNK pathway, independently of p53. PEITC-induced expression of DDB2 is critical for inhibition of tumor progression by PEITC. Tumors derived from DDB2-deficient colon cancer cells are refractory to PEITC-treatments, resulting from deficiencies in apoptosis and senescence. The DDB2-proficient tumors, on the other hand, respond effectively to PEITC. The results show that PEITC can be used to induce expression of DDB2, and that expression of DDB2 is critical for effective response of tumors to PEITC.

| S-EPMC3571992 | biostudies-literature

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