Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA225789 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Colon cancer is one of the most common tumors worldwide. Recent reports showed that patients treated with the antidepressant fluoxetine had reduced colon cancer risk, with effects similar to the chemotherapeutic 5-fluoro-uracil. Here, we examined the effects of fluoxetine and 5-fluoro-uracil on gene expression of HT29 colon cancer cell xenografts. HT29 xenografts in NOD/SCID mice were treated with vehicle (physiological solution), fluoxetine (30mg/kg/day), or 5-Fluoro-uracil (50 mg/kg/day).
2015-06-09 | E-GEOD-51904 | biostudies-arrayexpress
Project description:Colon cancer is one of the most common tumors worldwide. Recent reports showed that patients treated with the antidepressant fluoxetine had reduced colon cancer risk, with effects similar to the chemotherapeutic 5-fluoro-uracil. Here, we examined the effects of fluoxetine and 5-fluoro-uracil on gene expression of HT29 colon cancer cell xenografts.
2015-06-09 | GSE51904 | GEO
Project description:Selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine are the most common treatment for major depression. However, approximately 50% of depressed patients fail to achieve an effective treatment response. Understanding how gene expression systems relate to treatment responses may be critical for understanding antidepressant resistance. Transcriptome profiling allows for the simultaneous measurement of expression levels for thousands of genes and the opportunity to utilize this information to determine mechanisms underlying antidepressant treatment responses. However, the best way to relate this immense amount of information to treatment resistance remains unclear. We take a novel approach to this question by examining dentate gyrus transcriptomes from the perspective of a stereotyped fluoxetine-induced gene expression program. Expression programs usually represent stereotyped changes in expression levels that occur as cells transition phenotypes. Fluoxetine will shift transcriptomes so they lie somewhere between a baseline state and a full-response at the end of the program. The position along this fluoxetine-induced gene expression program (program status) was measured using principal components analysis (PCA). The same expression program was initiated in treatment-responsive and resistant mice but treatment response was associated with further progression along the fluoxetine-induced gene expression program. The study of treatment-related differences in gene expression program status represents a novel way to conceptualize differences in treatment responses at a transcriptome level. Understanding how antidepressant-induced gene expression program progression is modulated represents an important area for future research and could guide efforts to develop novel augmentation strategies for antidepressant treatment resistant individuals. 38 samples, 2 dentate regions (dorsal/ventral), 3 groups (control, antidepressant resistant (4 mice), antidepressant responsive (7 mice), untreated (8 mice).
2013-12-31 | E-GEOD-43261 | biostudies-arrayexpress
Project description:elective serotonin reuptake inhibitors (SSRIs) exhibit delayed therapeutic effects despite rapid serotonin elevation, suggesting their dependence on slow neuroplastic adaptations. Here, we demonstrate that antidepressant actions require cell type-specific translational regulation of the peptidergic signaling in the dentate gyrus (DG). Chronic, but not acute, treatment with an SSRI fluoxetine selectively enhances translational activity in hilar mossy cells (MCs), with no detectable changes in neighboring granule cells (GCs). Combining Translating Ribosome Affinity Purification (TRAP) with RNA sequencing revealed distinct baseline translatomes between these two glutamatergic neurons and identified fluoxetine-induced remodeling of peptidergic pathways in the DG. Crucially, we discovered MC-specific enrichment of the neuropeptide PACAP, which undergoes translation-dependent upregulation by chronic fluoxetine treatment. This PACAP induction mediates neuroadaptive plasticity in PAC1 receptor-expressing GCs and drives behavioral responses prominently in female mice during prolonged SSRI administration. Our findings establish cell type-specific translational reprogramming as a novel mechanistic framework for antidepressant action.
2026-05-27 | GSE309750 | GEO
Project description:We constructed a comprehensive multi-omics map of the molecular effects of fluoxetine (an SSRI antidepressant), in 27 rat brain regions. We profiled gene expression (bulk RNA-seq, 210 datasets) and chromatin state (bulk chromatin immunoprecipitation sequencing (ChIP-seq) for the histone marker H3K27ac, 100 datasets) in a broad, unbiased panel of 27 brain regions across the entire rodent brain, in naive and fluoxetine-treated animals. We complemented this approach with single-cell RNA-seq (scRNA-seq) analysis of two brain regions. Using diverse integrative data analysis techniques we characterized the complex and multifaceted effects of fluoxetine on region-specific and cell-type-specific gene regulatory networks and pathways. Remarkably, we observed profound molecular changes across the brain (>4,000 differentially expressed genes and differentially acetylated ChIP-seq peaks each) that were highly region-dependent. We leveraged this atlas to identify fluoxetine-moduated genes and gene-regulatory loci, predict enriched motifs that suggest potential upstream regulators, and validate global mechanisms of fluoxetine action.
2022-09-04 | GSE193040 | GEO
Project description:We constructed a comprehensive multi-omics map of the molecular effects of fluoxetine (an SSRI antidepressant) in 27 rat brain regions. We profiled gene expression (bulk RNA-seq, 210 datasets) and chromatin state (bulk chromatin immunoprecipitation sequencing (ChIP-seq) for the histone marker H3K27ac, 100 datasets) in a broad, unbiased panel of 27 brain regions across the entire rodent brain, in naive and fluoxetine-treated animals. We complemented this approach with single-cell RNA-seq (scRNA-seq) analysis of two brain regions (20 datasets). Remarkably, in the single-cell RNA-seq profiling we observed profound changes in the transcripts of hippocampal dorDG and venDG (~500 DEGs in specific cell types). Using diverse integrative data analysis techniques we characterized the complex and multifaceted effects of fluoxetine on region-specific and cell-type-specific gene regulatory networks and pathways. We leveraged this atlas to identify fluoxetine-modulated genes and gene-regulatory loci, predict enriched motifs that suggest potential upstream regulators, and validate global mechanisms of fluoxetine action.
2022-09-04 | GSE197622 | GEO
Project description:We constructed a comprehensive multi-omics map of the molecular effects of fluoxetine (an SSRI antidepressant), in 27 rat brain regions. We profiled gene expression (bulk RNA-seq, 210 datasets) and chromatin state (bulk chromatin immunoprecipitation sequencing (ChIP-seq) for the histone marker H3K27ac, 100 datasets) in a broad, unbiased panel of 27 brain regions across the entire rodent brain, in naive and fluoxetine-treated animals. We complemented this approach with single-cell RNA-seq (scRNA-seq) analysis of two brain regions. Using diverse integrative data analysis techniques we characterized the complex and multifaceted effects of fluoxetine on region-specific and cell-type-specific gene regulatory networks and pathways. Remarkably, we observed profound molecular changes across the brain (>4,000 differentially expressed genes and differentially acetylated ChIP-seq peaks each) that were highly region-dependent. We leveraged this atlas to identify fluoxetine-moduated genes and gene-regulatory loci, predict enriched motifs that suggest potential upstream regulators, and validate global mechanisms of fluoxetine action.
2022-09-04 | GSE194289 | GEO
Project description:Here, we performed a high-throughput drug screening and identified fluoxetine, originally an FDA-approved antidepressant, as candidate therapeutic agent for NEPC. In vitro experiments revealed that fluoxetine effectively curbed the neuroendocrine differentiation and inhibited the cell viability by targeting the AKT pathway. Altogether, this work repurposed fluoxetine for antitumor application, and supported its clinical development for NEPC therapy, which may provide a promising therapeutic strategy.
2023-04-05 | GSE224715 | GEO
Project description:Selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine are the most common treatment for major depression. However, approximately 50% of depressed patients fail to achieve an effective treatment response. Understanding how gene expression systems relate to treatment responses may be critical for understanding antidepressant resistance. Transcriptome profiling allows for the simultaneous measurement of expression levels for thousands of genes and the opportunity to utilize this information to determine mechanisms underlying antidepressant treatment responses. However, the best way to relate this immense amount of information to treatment resistance remains unclear. We take a novel approach to this question by examining dentate gyrus transcriptomes from the perspective of a stereotyped fluoxetine-induced gene expression program. Expression programs usually represent stereotyped changes in expression levels that occur as cells transition phenotypes. Fluoxetine will shift transcriptomes so they lie somewhere between a baseline state and a full-response at the end of the program. The position along this fluoxetine-induced gene expression program (program status) was measured using principal components analysis (PCA). The same expression program was initiated in treatment-responsive and resistant mice but treatment response was associated with further progression along the fluoxetine-induced gene expression program. The study of treatment-related differences in gene expression program status represents a novel way to conceptualize differences in treatment responses at a transcriptome level. Understanding how antidepressant-induced gene expression program progression is modulated represents an important area for future research and could guide efforts to develop novel augmentation strategies for antidepressant treatment resistant individuals.
2013-12-31 | GSE43261 | GEO
Project description:A Multi-omics Comparison Unveils Convergent and Divergent Antidepressant Mechanisms of Fluoxetine and St. John's Wort extract
| PXD067684 |