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Genistein Cooperates with the Histone Deacetylase Inhibitor Vorinostat to Induce Cell Death in Prostate Cancer Cells (methylation data)

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE35245 | GEO | 2012/12/01

SECONDARY ACCESSION(S): PRJNA156033

REPOSITORIES: GEO

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Genistein Cooperates with the Histone Deacetylase Inhibitor Vorinostat to Induce Cell Death in Prostate Cancer Cells (expression data)

2012-12-01 | GSE35242 | GEO

Genistein Cooperates with the Histone Deacetylase Inhibitor Vorinostat to Induce Cell Death in Prostate Cancer Cells (expression data)

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

Genistein Cooperates with the Histone Deacetylase Inhibitor Vorinostat to Induce Cell Death in Prostate Cancer Cells (methylation data)

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

Genistein treatment effects upin human prostate

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

Genome-wide DNA methylation profiling of prostate specimens from a clinical trial of genistein supplementation prior to prostatectomy.

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

Genome-wide expression profiling of prostate specimens from a clinical trial of genistein supplementation prior to prostatectomy.

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

Genistein treatment effects upin human prostate

Project description:Genistein treatment effects upin human prostate

| PRJNA527197 | ENA

RNA profiling of genistein and Tanshinone I treated cervical cancer cells

Project description:Phenotypically, we observed that both genistein and Tanshinone I exert the inhibitory effects on the proliferation and metastasis of cervical cancer. The aim of this study was to comprehensively decipher the anti-metastasis effect and molecular mechanism of genistein and Tanshinone I on the cervical cancer. The results showed that genistein and Tanshinone I strongly change the RNA profiling of the cervical cancer cells in different manners: genistein mainly targets on regulation of RNA transcription, central carbon metabolism in cancer, microRNAs in cancer and focal adhesion etc; Tanshinone I mainly effects on central carbon metabolism in cancer, mitophagy process.

2022-10-31 | GSE159893 | GEO

Quantitative Phosphoproteomics Reveals Genistein as a Modulator of Cell Cycle and DNA Damage Response Pathways

Project description:Around one sixth of breast cancer cases are classified as triple-negative breast cancer (TNBC), named after the absence of the expression of estrogen receptors (ER), progesterone receptors (PR), and human epidermal growth factor receptor 2 (HER2); however, patients with TNBC suffer from poor clinical outcome and shortage of targeted therapy. Genistein, an estrogenic soy isoflavone, shows anti-cancer effects in TNBC cells such as inducing G2/M cell cycle arrest and apoptosis. However, the underlying mechanism of its anti-cancer effects is poorly understood and its elucidation can help the development of novel therapeutic strategies for TNBC. In this study, by combining isobaric tag-based TMT labeling with titanium dioxide-based phosphopeptide enrichment, we quantitated 5,445 phosphorylation sites on 2,008 phosphoproteins in a TNBC cell line, MDA-MB-231, upon genistein treatment. Our analysis revealed 332 genistein-regulated phosphorylation sites on 226 proteins. Our data show that genistein can regulate several biological processes during the cell cycle, including DNA replication, cohesin complex cleavage, and kinetochore formation. In the meantime, genistein can also activate DNA damage response, including activation of ATR and BRCA1 complex. Overall, for the first time, our study present the evidence that genistein could inhibit TNBC cell growth by regulating the cell cycle and DNA damage response. Our findings help elucidate the mechanisms through which genistein exerts its anti-cancer effects in TNBC cells.

2016-01-26 | PXD002735 | Pride

Gene Expression Profiling of Gemcitabine, Genistein and Combinatorial Effects on Pancreatic Cancer Cell Lines

Project description:We reported the transcriptional effects of gemcitabine, genistein and the combined gemcitaibe/gensitein treatments on two pancreatic cancer cell lines MiaPaCa2 and PANC1. The overall purpose of the study to understand the underlying mechanism of genistein chemoenhancing function.

2019-12-31 | GSE97766 | GEO

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