Gene expression signatures for apigenin treatment in human AML cell lines
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ABSTRACT:
PROVIDER: PRJNA798012 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the effect of apigenin on gene expression, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to suppress the cell proliferation of human acute myeloid leukemia (AML) cell lines. HL-60 amn NB4 cells were treated with apigenin for 24 h in vitro.
2022-03-31 | GSE193798 | GEO
Project description:Single-shot proteome analysis of 4 AML cell lines; 2 selinexor sensitive cell lines (GDM-1, MV4-11) and 2 resistant cell lines (NOMO-1 and PL-21) and ex vivo AML cells from 30 patients treated with DMSO (B; before treatment) or 1 uM selinexor (A; after treatment) for 6 hours.
2022-08-07 | PXD033515 | Pride
Project description:The changes of mature microRNA expression levels after apigenin treatment on Huh7 cells were determined. Huh7 cells were treated with 10microM apigenin for 24hr and the changes of global mature microRNA expression levels were determined.
2013-08-20 | E-GEOD-46526 | biostudies-arrayexpress
Project description:The changes of mature microRNA expression levels after apigenin treatment on Huh7 cells were determined.
2013-08-20 | GSE46526 | GEO
Project description:In vitro study with AML cell lines that are treated with different concentrations of cytarabine (nucleoside analog). 8 AML cell lines were incubated for 24hr with 0uM, 1uM and 10uM ara-C. After 24hr the cells were washed and pellets were stored in -80°C for genomic and metabolomic analysis.
2018-08-02 | MSV000082685 | GNPS
Project description:Age is the primary risk factor for many chronic diseases and cognitive decline during brain aging may increase dementia risk. Hallmarks of brain aging including neuronal dysfunction and glial contribute to reduced cognitive function, and there is a persistent lack of effective treatments. Bioactive plant compounds called “nutraceuticals” can target age-related cellular processes and may protect cognitive function. Apigenin is a flavone found in plants such as chamomile and can inhibit hallmarks of aging such as cellular senescence, mitochondrial dysfunction, and impaired proteostasis. However, the underlying mechanisms of apigenin in the brain are not fully understood. Here, we characterized brain transcriptome changes in young and old mice given apigenin in drinking water and examined potential mechanisms in human astrocytes. Consistent with previous studies, we observed improved novel object recognition in old mice treated with apigenin versus old controls. Transcriptome analyses in old controls found differentially expressed genes related to immune responses, inflammation, and cytokine regulation versus young. Fewer differences were observed in old apigenin-treated versus old controls, but these changes were related to development, behavior, and antiviral responses. The majority of upregulated genes in old mice were downregulated with apigenin treatment and associated with immune responses. Similarly, the genes that were reduced with aging, but increased in old apigenin-treated mice were related to pathways important for neurological function/disease, cellular maintenance, and homeostatic signaling. We also found that glial cells drove the majority of the transcriptome differences with aging and apigenin-treatment. To explore the mechanism of action for apigenin in glial cells, we treated replicatively aged astrocytes with apigenin and observed reduced markers of inflammation and cellular senescence. Collectively, our data support the role of apigenin as a protector of cognitive and neuronal function protectant through the suppression of neuroinflammatory genes and proteins and may be especially important in non-neuronal cells.
2024-02-14 | GSE232201 | GEO
Project description:In vitro study with AML cell lines that are treated with different concentrations of cytarabine (nucleoside analog). 8 AML cell lines were incubated for 24hr with 0uM, 1uM and 10uM ara-C. After 24hr the cells were washed and pellets were stored in -80°C for genomic and metabolomic analysis.
2015-02-15 | ST000288 | MetabolomicsWorkbench
Project description:There is no known single therapeutic drug for treating hypercholesterolemia that comes with negligible systemic side effects. In the current study, using next generation RNA sequencing approach in mouse embryonic fibroblasts we discovered that two structurally related flavonoid compounds, Apigenin and Chrysin exhibited moderate blocking ability of multiple transcripts that regulate rate limiting enzymes in the cholesterol biosynthetic pathway. The observed decrease in cholesterol biosynthesis pathway correlated well with an increase in transcripts involved in generation and trafficking of ketone bodies as evident by the upregulation of Bdh1 and Slc16a6 transcripts. Impact statement - The hypocholesterolemic potential of Apigenin and Chrysin at higher concentrations along with their ability to generate ketogenic substrate especially during embryonic stage is useful or detrimental for embryonic health is not clear and still debatable. Our findings will set the stage for translating this information to whole animal and clinical studies that could shed light to the existing information regarding safe use of Apigenin and Chrysin, specifically to embryonic health.
2021-08-09 | GSE155852 | GEO
Project description:Cancer cells adapt to treatment, leading to the emergence of clones that are more aggressive and resistant to anti-cancer therapies. We have a limited understanding of the evolution of treatment resistance as we have lacked technologies to map the evolution of cancer under the selective pressures. To address this, we developed a hierarchical, dynamic lineage tracing method called FLARE (Following Lineage Adaptation and Resistance Evolution). We use this technique to track the progression of acute myeloid leukemia (AML) cell lines through exposure to Cytarabine (AraC), a front-line treatment in AML, in vitro and in vivo. We map distinct cellular lineages in murine and human AML cell lines that are predisposed to AraC persistence and/or resistance via upregulation of cell adhesion and motility pathways. Additionally, we highlight heritable increased expression of immunoproteasome 11S regulatory cap subunits as a potential mechanism aiding AML cell survival, proliferation, and immune escape in vivo. Finally, we validate the clinical relevance of these signatures in the TARGET-AML cohort, with a bisected response in blood and bone marrow. Our findings reveal a broad spectrum of resistance signatures attributed to significant cell transcriptional changes, and we expect this high-resolution profiling of treatment response to be a useful tool to dissect the evolution of treatment response in a wide range of tumor types.
2025-02-12 | GSE289459 | GEO
Project description:Cancer cells adapt to treatment, leading to the emergence of clones that are more aggressive and resistant to anti-cancer therapies. We have a limited understanding of the evolution of treatment resistance as we have lacked technologies to map the evolution of cancer under the selective pressures. To address this, we developed a hierarchical, dynamic lineage tracing method called FLARE (Following Lineage Adaptation and Resistance Evolution). We use this technique to track the progression of acute myeloid leukemia (AML) cell lines through exposure to Cytarabine (AraC), a front-line treatment in AML, in vitro and in vivo. We map distinct cellular lineages in murine and human AML cell lines that are predisposed to AraC persistence and/or resistance via upregulation of cell adhesion and motility pathways. Additionally, we highlight heritable increased expression of immunoproteasome 11S regulatory cap subunits as a potential mechanism aiding AML cell survival, proliferation, and immune escape in vivo. Finally, we validate the clinical relevance of these signatures in the TARGET-AML cohort, with a bisected response in blood and bone marrow. Our findings reveal a broad spectrum of resistance signatures attributed to significant cell transcriptional changes, and we expect this high-resolution profiling of treatment response to be a useful tool to dissect the evolution of treatment response in a wide range of tumor types.
2025-02-12 | GSE289454 | GEO