Genistein treatment effects upin human prostate
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ABSTRACT:
PROVIDER: PRJNA527197 | ENA |
REPOSITORIES: ENA
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Project description:Prior studies support the notion that the experimental chemopreventive agent, genistein, inhibits prostate cancer (PCa) cell movement in humans and that this in turn inhibits metastatic spread, thereby preventing PCa-specific death. As many effects have been ascribed to genistein, it has been considered a non-specific agent. However, its effects are concentration-dependent, and the vast majority of studies use concentrations greater than 3 logs above those associated with dietary consumption. Genistein is found in soy, and individuals consuming soy-based diets have blood concentrations of free genistein in the low nanomalar range. Using dosing guided by phase I pharmacokinetic studies in US men, prospective treatment of men on a phase II trial with genistein for one month prior to radical prostatectomy for localized PCa. Here we conducted an unbiased screening for effects of genistein in prostate as well as evaluate changes between normal and cancer cells.
2019-03-16 | GSE128339 | GEO
Project description:To identify molecular effects of genistein on mRNA levels in prostate cancer, we compared gene expression profiles of genistein-treated tumors with placebo-treated samples. There were 628 probes that reached nominally significant p-values. The genes that were differentially expressed between genistein and placebo samples were involved in angiogenesis, apoptosis, epithelial to mesenchymal transition, and tumor progression. Gene enrichment analysis suggested that PTEN and PDGF were activated, while MYC, beta-estradiol, glucocorticoid receptor NR3C1, and interferon-gamma were repressed in response to genistein treatment. These findings highlight the effects of genistein on global changes in gene expression in prostate cancer and its effects on molecular pathways involved in prostate tumorigenesis.
2017-06-23 | GSE84748 | GEO
Project description:We have investigated the effects of genistein on several prostate cancer cell lines, including the ARCaP-E/ARCaP-M model of the epithelial-to-mesenchymal transition (EMT), to analyze effects on their epigenetic state. In addition, we investigated the effects of combined treatment of genistein with the histone deacetylase inhibitor vorinostat on survival in prostate cancer cells. Using whole-genome expression profiling and whole-genome methylation profiling, we have determined the genome-wide differences in genetic and epigenetic responses to genistein in prostate cancer cells before and after undergoing the EMT. Also, cells were treated with genistein, vorinostat, and a combination treatment, where cell death and cell proliferation was determined.
2012-12-01 | GSE35245 | GEO
Project description:We have investigated the effects of genistein on several prostate cancer cell lines, including the ARCaP-E/ARCaP-M model of the epithelial-to-mesenchymal transition (EMT), to analyze effects on their epigenetic state. In addition, we investigated the effects of combined treatment of genistein with the histone deacetylase inhibitor vorinostat on survival in prostate cancer cells. Using whole-genome expression profiling and whole-genome methylation profiling, we have determined the genome-wide differences in genetic and epigenetic responses to genistein in prostate cancer cells before and after undergoing the EMT. Also, cells were treated with genistein, vorinostat, and a combination treatment, where cell death and cell proliferation was determined.
2012-12-01 | GSE35242 | GEO
Project description:We have investigated the effects of genistein on several prostate cancer cell lines, including the ARCaP-E/ARCaP-M model of the epithelial-to-mesenchymal transition (EMT), to analyze effects on their epigenetic state. In addition, we investigated the effects of combined treatment of genistein with the histone deacetylase inhibitor vorinostat on survival in prostate cancer cells. Using whole-genome expression profiling and whole-genome methylation profiling, we have determined the genome-wide differences in genetic and epigenetic responses to genistein in prostate cancer cells before and after undergoing the EMT. Also, cells were treated with genistein, vorinostat, and a combination treatment, where cell death and cell proliferation was determined. ARCAP-E, ARCAP-M, and normal human PrEC cells were analyzed for genome-wide methylation using the Illumina 27K CpG Methylation BeadChip. ARCAP-E and ARCAP-M cells were treated with DMSO as a negative control, genistein, or 5-aza-deoxycytidine as a positive control for demethylation. PrEC cells, used as a normal human prostate cell line control, were untreated.
2012-12-01 | E-GEOD-35245 | biostudies-arrayexpress
Project description:We have investigated the effects of genistein on several prostate cancer cell lines, including the ARCaP-E/ARCaP-M model of the epithelial-to-mesenchymal transition (EMT), to analyze effects on their epigenetic state. In addition, we investigated the effects of combined treatment of genistein with the histone deacetylase inhibitor vorinostat on survival in prostate cancer cells. Using whole-genome expression profiling and whole-genome methylation profiling, we have determined the genome-wide differences in genetic and epigenetic responses to genistein in prostate cancer cells before and after undergoing the EMT. Also, cells were treated with genistein, vorinostat, and a combination treatment, where cell death and cell proliferation was determined. ARCaP-E and ARCaP-M cells were analyzed for whole genome expression using the Illumina HumanHT-12 Expression BeadChip. Samples were treated with DMSO control, genistein, vorinostat, a combination of vorinostat and genistein, or 5-aza-deoxycytidine. Samples were prepared in triplicate on independent days.
2012-12-01 | E-GEOD-35242 | biostudies-arrayexpress
Project description:To identify molecular effects of genistein on DNA methylation in prostate cancer, we compared DNA methylation profiles of genistein-treated tumors with placebo-treated samples. There were 156 probes with significantly increased methylation in placebo-treated cases versus normal tissues that were not significant between genistein-treated cases and normal tissues, suggesting that genistein may have had some demethylation effects. These 156 probes corresponded to at least 92 separate genes including ADCY4, ALOX12, HAAO, LRRC4, NEU1, RAPGEFL1, and WNT7B.These findings highlight the effects of genistein on global changes in DNA methylation in prostate cancer and its effects on molecular pathways involved in prostate tumorigenesis.
2017-06-23 | GSE84749 | GEO
Project description:Gene expression profiling to identify genes significantly modulated by low and high doses of genistein in LNCaP cells. Significant genes were identified using StepMiner analysis and significantly altered pathways with Ingenuity Pathways analysis. Genistein significantly altered expression of transcripts involved in cell growth, carcinogen defenses and steroid signaling pathways. The effects of genistein on these pathways were confirmed by directly assessing dose-related effects on LNCaP cell growth, NQO-1 enzymatic activity and PSA protein expression. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed.
2010-10-30 | E-GEOD-24796 | biostudies-arrayexpress
Project description:Gene expression profiling to identify genes significantly modulated by low and high doses of genistein in LNCaP cells. Significant genes were identified using StepMiner analysis and significantly altered pathways with Ingenuity Pathways analysis. Genistein significantly altered expression of transcripts involved in cell growth, carcinogen defenses and steroid signaling pathways. The effects of genistein on these pathways were confirmed by directly assessing dose-related effects on LNCaP cell growth, NQO-1 enzymatic activity and PSA protein expression.
2010-10-20 | GSE24796 | GEO
Project description:Androgen signalling through the androgen receptor (AR) plays a critical role in prostate cancer (PCa) initiation and progression. Estrogen and the estrogen receptor, in synergy with androgen, are essential for cell growth of the normal and malignant prostate. However, the exact role that estrogen plays in prostate carcinogenesis, and the precise mechanisms involved, remain unclear. We have previously demonstrated the metastasis-promoting effect of an estrogen receptor Beta (ERβ) agonist (genistein) and the inhibitory action of an anti-estrogen (ICI 182, 780) in patient-derived PCa xenograft models mimicking localized and metastatic disease. In this study, we compared the gene expression profiles of treated and untreated PCa xenografts using microarrays to identify a unique set of genes that were both up-regulated by genistein treatment and down-regulated by the anti-estrogen, ICI 182,780. Five of the six genes identified from this comparison belonged to the metallothionein (MT) gene family. Knock-down of ERβ led to a reduction in MT gene expression, confirming its role in regulating these genes. Using qRT-PCR, the differences in expression levels were validated in the metastatic and non-metastatic LTL313 PCa xenograft tumour lines, both of which were originally derived from the same PCa patient. Together our data provides evidence for the role of ERβ signalling in PCa metastasis and implicates estrogen-stimulated MT gene expression in this process. Three samples each (total RNA extracted from three tumours of three different animals from each group) for control, genistein and ICI were used for the array.
2012-12-27 | E-GEOD-43146 | biostudies-arrayexpress