Apigenin inhibits tumor angiogenesis by suppressing microvesicle biogenesis
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ABSTRACT:
PROVIDER: PRJNA1055490 | ENA |
REPOSITORIES: ENA
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Project description:Apigenin regulates multiple pathways related to microvesicle biogenesis without affecting the expression of small Rho GTPase activator guanine nucleotide exchange factors (GEFs). However, apigenin can primarily targets ARHGEF1 protein, a GEF of the small GTPases, thereby inhibiting the activity of small G proteins such as Cdc42, which is essential in regulating the signaling for the release of microvesicles from tumor cells. Targeting ARHGEF1, apigenin effectively prevents tumor cells from releasing microvesicles. This, in turn, inhibits tumor angiogenesis related to VEGF90K transport on microvesicles, ultimately impeding tumor progression.
2024-07-22 | GSE251817 | GEO
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:Aging causes dysfunctional changes to the bone microenvironment that lead to osteoporosis development. Osteoporosis is a serious bone health issue that is characterized by decreased bone formation and increased bone resorption. The aim of this study is to evaluate the effects of natural compounds, Apigenin and Rutaecarpine on osteoblast differentiation and examine if Apigenin and Rutaecarpine can rescue osteogenesis in aging-context. Using human bone marrow stromal cell line (hBMSCs) and primary cells obtained from young and aged women, we showed that Apigenin and Rutaecarpine are potent in inducing osteoblast differentiation and mineralization. These compounds were able to reduce senescence along with their impacts on suppressing oxidative stress and inflammation, which both contribute to aging and bone metabolic dysfunctions. Our microarray-based transcription profiling of hBMSC-derived osteoblasts treated with either 1 µM of Apigenin or Rutaecarpine during osteoblast differentiation for 21 days revealed distinct impacts of Apigenin and Rutaecarpine on different genes including those involved in bone metabolism and skeletal system development. Additionally, Ex-vivo organotypic embryonic chick-femur culture model was used to determine the osteogenic effects of Apigenin and Rutaecarpine. The average bone volume and cortical thickness of these chick femurs were both increased significantly by Apigenin and Rutaecarpine. Collectively, our study provides a novel insight for developing therapeutic strategies using natural compounds to combat aging and its effect on bone health.
2024-03-20 | GSE252845 | GEO
Project description:Differential gene expression in mice liver after apigenin administration. Gene expression from control mice were compared with apigenin treated mice at different dose level.
2011-04-27 | GSE12716 | GEO
Project description:Differential gene expression in mice liver after apigenin administration. Gene expression from control mice were compared with apigenin treated mice at different dose level. To study differential expression primarily at high stringency and in dose dependent manner was to increase the statistical confidence in the detection of important genes and cellular processes with a probable role in the initiation and propagation of toxicity as well as those possibly involved in regeneration during the early phase of tissue response.
2011-04-27 | E-GEOD-12716 | biostudies-arrayexpress
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:The changes of mature microRNA expression levels after apigenin treatment on Huh7 cells were determined.
2013-08-20 | GSE46526 | GEO
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: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:Neovascularization contributes to multiple visual disorders including age-related macular degeneration (AMD). Current therapies for treating ocular angiogenesis are centered on the inhibition of vascular endothelial growth factor (VEGF). While clinically effective, some AMD patients are refractory or develop resistance to anti-VEGF and concerns of increased risks of developing geographic atrophy following long-term treatment have been raised. Identification of alternative pathways to inhibit pathological angiogenesis is thus important. We have identified a novel inhibitor of angiogenesis, COCO/DAND5, a member of the Cerberus-related DAN family. We demonstrate that COCO inhibits sprouting, migration and cellular proliferation of cultured endothelial cells. Intravitreal injections of COCO inhibited retinal vascularization during development and in models of retinopathy of prematurity and AMD. COCO equally abrogated angiogenesis in choroid explants and in a model of choroidal neovascularization. Mechanistically, COCO inhibited the expression of TGFβ and BMP pathwaysand altered ATP production, glucose uptake and redox balance of endothelial cells. Together, these data show that COCO is an inhibitor of retinal and choroidal angiogenesis, possibly representing a therapeutic option for the treatment of neovascular ocular diseases.
2020-12-22 | GSE160099 | GEO