Ontology highlight
ABSTRACT:
PROVIDER: PRJNA152811 | ENA |
REPOSITORIES: ENA
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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: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:Genistein Cooperates with the Histone Deacetylase Inhibitor Vorinostat to Induce Cell Death in Prostate Cancer Cells (expression data)
| PRJNA156031 | ENA
Project description:Genistein Cooperates with the Histone Deacetylase Inhibitor Vorinostat to Induce Cell Death in Prostate Cancer Cells (methylation data)
| PRJNA156033 | ENA
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:Combining different clinical agents to target multiple pathways in prostate cancer cells, including androgen receptor (AR) signaling, is potentially an effective strategy to improve outcomes for men with metastatic disease. We have previously demonstrated that sub-effective concentrations of an AR antagonist, bicalutamide, a histone deacetylase inhibitor, vorinostat (SAHA), and a hsp90 inhibitor, 17-AAG, act synergistically when combined to cause death of AR-dependent prostate cancer cells. In this study, expression profiling of human prostate cancer cells treated with bicalutamide, vorinostat (SAHA) or 17-AAG, alone or in paired combination, was employed to determine the molecular mechanisms underlying these synergistic interactions. We used microarray analysis to determine the global molecular profile contributing to the synergistic cell death in LNCaP human prostate cancer cells caused by combinations of bicalutamide, vorinostat (SAHA), or 17-AAG. LNCaP human prostate cancer cells were treated for 6 hours with drug treatments as follows: vehicle control, 5 uM bicalutamide, 1 uM vorinostat (SAHA), 40 nM 17-AAG, 5 uM bicalutamide + 40 nM 17-AAG, 40 nM 17-AAG + 1 uM vorinostat (SAHA), or 5 uM bicalutamide + 1 uM vorinostat (SAHA). Each treatment was performed in sextuplicate.
2014-03-27 | E-GEOD-56188 | biostudies-arrayexpress
Project description:Combining different clinical agents to target multiple pathways in prostate cancer cells, including androgen receptor (AR) signaling, is potentially an effective strategy to improve outcomes for men with metastatic disease. We have previously demonstrated that sub-effective concentrations of an AR antagonist, bicalutamide, a histone deacetylase inhibitor, vorinostat (SAHA), and a hsp90 inhibitor, 17-AAG, act synergistically when combined to cause death of AR-dependent prostate cancer cells. In this study, expression profiling of human prostate cancer cells treated with bicalutamide, vorinostat (SAHA) or 17-AAG, alone or in paired combination, was employed to determine the molecular mechanisms underlying these synergistic interactions. We used microarray analysis to determine the global molecular profile contributing to the synergistic cell death in LNCaP human prostate cancer cells caused by combinations of bicalutamide, vorinostat (SAHA), or 17-AAG.
2014-03-27 | GSE56188 | GEO
Project description:This study is an open label non randomized study of hydroxychloroquine (HCQ) with histone deacetylase (HDAC) inhibitor Vorinostat in patients with advanced solid tumors to determine the maximum tolerated dose (MTD) and to evaluate the safety and antitumor activity of this drug combination.
| 2081555 | ecrin-mdr-crc
Project description:We aimed to investigate gene expression associated with radiosensitisation of normoxic and hypoxic prostate cancer cells by the class I/II histone deacetylase inhibitor (HDACi) vorinostat. A pronounced deregulation of DNA repair and chromatin organization genes by vorinostat in DU 145 than in PC-3 or 22Rv1 was found and was a likly mechanism underlying radiosensitisation of DU 145. Expression of these genes was generally not affected by hypoxia and was altered by vorinostat in DU 145 towards the baseline levels of PC-3 and 22Rv1. A 56-gene expression signature associated with radiosensitisation under normoxia and hypoxia, including 8 genes with baseline expression characteristic of the radiosensitising effect was generated. These findings propose a hypoxia independent expression signature to predict the radiosensitising effect of vorinostat.
2016-12-08 | GSE80657 | GEO