Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA159569 | ENA |
REPOSITORIES: ENA
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Project description:For a long time, the BARD1 (BRCA1-associated RING domain 1) protein has been considered as a BRCA1 (BReast Cancer susceptibility gene 1, early onset) interactor, and tumor suppressor mutated in breast and ovarian cancers. Despite its functions in a stable heterodimer with BRCA1, there is increasing evidence for BRCA1-independent functions of BARD1. Here, we investigated BARD1 expression and function in human acute myeloid leukemias and their modulation by epigenetic mechanisms and microRNA. We show that the HDACi (histone deacetylase inhibitor) Vorinostat reduces BARD1 mRNA levels by increasing miR-19a and miR-19b expression levels. Moreover, we identify specific BARD1 isoforms that might act as tumor diagnostic and prognostic markers. Two-condition experiment: untreated NB4 cells (control) vs. NB4 cells treated with 5M-BM-5M SAHA (Vorinostat) for 6h. Biological replicates: 3 control, 3 treated, independently grown and harvested at 6 hours. One replicate per array.
2014-12-22 | E-GEOD-37374 | 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:To investigate whether microRNAs (miRNAs) were induced by histone deacetylase inhibitors (HDACi) in human gastric cancer cells, the miRNA-seq was used to screen differentially expressed miRNAs in two human gastric cancer cell lines (HGC-27 and AGS) treated with the HDACi vorinostat (SAHA) or vehicle (DMSO).
2024-06-20 | GSE178644 | GEO
Project description:Transcriptional profiling of U937 miR-194-5p (UmiR-194-5p) vs U937 miR-194-5p (UmiR-194-5p) treated with SAHA (Vorinostat; suberoylanilide hydroxamic acid) for 24 h at 5uM concetration
2017-05-22 | GSE73648 | GEO
Project description:AML cell lines (K562, U937 and NB4) were treated with MS27-275 (MS) and SAHA for 6 hours and the gene expression analysis revealed commonly regulated genes by the 2 HDACi. AML blasts were treated with SAHA for 6 hours and gene expression profiles were compared to commonly regulated genes by MS and SAHA in AML cell lines. The analysis revealed commonly regulated genes in these systems by SAHA.
2017-03-01 | GSE54871 | GEO
Project description:miRNA expression profiling of K562 ctrl vs K562 treated Saha 5 µM 6h
2017-05-22 | GSE69958 | GEO
Project description:miRNA expression profiling of U937 ctrl vs U937 treated Saha 5 µM 6h
2017-05-22 | GSE69957 | GEO
Project description:The biological active cargo of leukemia-derived extracellular vesicles (EVs) favours a wide variety of cancer-supportive mechanisms, including aberrant proliferative signalling, immune escape and drug resistance. However, whether and in which extent anti-neoplastic drugs affect EV cargo sorting is often underestimated. Vorinostat, also known as SAHA, has shown promising results against leukemia , and reached important clinical goals when combined with other therapeutics. Nevertheless, SAHA-mediated effects on intercellular communication via EVs remains unknown. Here, we found SAHA to significantly affects the overall cargo associated with leukemia-derived EVs. Interestingly, SAHA differently affects the intracellular and vesicular levels of miR194-5p and BCLAF1 ratio, which imbalance was previously shown to regulate cell survival and differentiation in leukemic cells. Moreover, in silico evaluations predicted SAHA to skew the tumoral potential ascribed to leukemic EVs, hypothesis confirmed by functional evaluations. Finally, EVs from SAHA-treated leukemic cells may condition the sensitivity of surrounding cancer cells to other antineoplastic agents. Altogether we showed that SAHA leads leukemic cells towards apoptosis while reverting the oncologic significance ascribed to leukemia-derived EVs, eventually affecting the efficacy, and therefore selection, of other therapeutics to use for combinatorial purposes.
2025-05-06 | PXD042168 | Pride