Effects of cordycepin on murine macrophage-like cells in the presence and absence of an inflammatory stimulus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA521157 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To perform high-throughput, transcriptome-wide analysis on RAW 264.7 cells treated with cordycepin with and without bacterial lipopolysaccharide (LPS) to investigate cordycepin's anti-inflammatory properties and determine whether particular classes of RNAs were sensitive to cordycepin.
2019-02-07 | GSE126157 | GEO
Project description:Cordycepin was widely considered as a direct tumor-suppressive drug, however, and as of now few studies have been presented to investigate the effect of cordycepin therapy to the tumor microenvironment (TME). In our study, we demonstrated that cordycepin would decrease the function of M1-like macrophage in TME, and also contribute to macrophage polarization (M2-macrophage). Herein, we tried to establish a combined therapeutic strategy of cordycepin and anti-CD47 antibody. Using single cell RNA sequencing, we improved that the combined treatment would significantly increase the effect of cordycepin, which would reactivate macrophages and reverse macrophage polarization. And then, the combined treatment would regulate the proportion of CD8+T cells to increase the PFS for digestive tract malignancy patients. Finally, Flow cytometry was used to validate the change of percentage for TAM and TIL. Our finding suggests the combined treatment of cordycepin and anti-CD47 mAb could significantly increase tumor suppression, which could increase M1-macrophage and decrease M2-macrophage. The PFS for digestive tract malignancy patients would be increased though regulation of CD8+T cells.
2023-03-30 | GSE224945 | GEO
Project description:Cordycepin (3â deoxyadenosine) is a biologically active compound that, when incorporated during RNA synthesis in vitro, provokes chain termination due to the absence of a 3â hydroxyl moiety. We were interested in the effects mediated by this drug in vivo and analysed its impact on RNA metabolism of yeast. Our results support the view that cordycepin-triphosphate (CoTP) is the toxic component that is limiting cell growth through inhibition of RNA synthesis. Unexpectedly, cordycepin treatment modulated 3â end heterogeneity of ACT1 and ASC1 mRNAs and rapidly induced extended transcripts derived from CYH2 and NEL025c loci. Moreover, cordycepin ameliorated the growth defects of poly(A) polymerase mutants and the pap1-1 mutation neutralized the effects of the drug on gene expression. Our observations are consistent with an epistatic relationship between poly(A) polymerase function and cordycepin action and suggest that a major mode of cordycepin activity reduces 3â end formation efficiency independently of its potential to terminate RNA chain elongation. Finally, chemical-genetic profiling revealed genome-wide pathways linked to cordycepin activity and identified novel genes involved in poly(A) homeostasis. Keywords: response to drug treatment Each experiment was performed as triplicate. We analyzed RNA obtained from wild-type cells, from wild-type cells treated with 40 microgram/ml cordycepin for 1 hour, from pap1-1 mutant cells grown at permissive temperature (25°C) and from pap1-1 mutant cells grown at permissive temperature (25°C) treated with 40 microgram/ml cordycepin for 1 hour.
2010-05-06 | E-GEOD-14619 | biostudies-arrayexpress
Project description:3’deoxyadenosine, also known as cordycepin, has been widely researched as a potential treatment for cancer, yielding promising results in tissue culture as well as in pre-clinical models. A wide variety of mechanisms of action have been proposed, with little agreement between different studies. Here, we confirm that cordycepin triphosphate is likely to be the active metabolite of cordycepin. Data from single and high throughput experiments showed that cordycepin represses growth factor induced gene expression. Bioinformatic analysis, quantitative PCR and western blotting confirmed that cordycepin blocks the PI3K/AKT/mTOR and/or MEK/ERK pathways in 6 cell lines. Effects of cordycepin on translation through mTOR pathway repression were detectable within 30 minutes, indicating a rapid process. Our data show that cordycepin has a broadly similar mechanism of action in all cell lines studied and indicate that its therapeutic target is a cordycepin triphosphate sensitive molecule that is required for growth factor signal transduction.
2025-02-19 | GSE277765 | GEO
Project description:Cordycepin (3’ deoxyadenosine) is a biologically active compound that, when incorporated during RNA synthesis in vitro, provokes chain termination due to the absence of a 3’ hydroxyl moiety. We were interested in the effects mediated by this drug in vivo and analysed its impact on RNA metabolism of yeast. Our results support the view that cordycepin-triphosphate (CoTP) is the toxic component that is limiting cell growth through inhibition of RNA synthesis. Unexpectedly, cordycepin treatment modulated 3’ end heterogeneity of ACT1 and ASC1 mRNAs and rapidly induced extended transcripts derived from CYH2 and NEL025c loci. Moreover, cordycepin ameliorated the growth defects of poly(A) polymerase mutants and the pap1-1 mutation neutralized the effects of the drug on gene expression. Our observations are consistent with an epistatic relationship between poly(A) polymerase function and cordycepin action and suggest that a major mode of cordycepin activity reduces 3’ end formation efficiency independently of its potential to terminate RNA chain elongation. Finally, chemical-genetic profiling revealed genome-wide pathways linked to cordycepin activity and identified novel genes involved in poly(A) homeostasis. Keywords: response to drug treatment
2009-01-30 | GSE14619 | GEO
Project description:3’deoxyadenosine, also known as cordycepin, has been widely researched as a potential treatment for cancer, yielding promising results in tissue culture as well as in pre-clinical models. A wide variety of mechanisms of action have been proposed, with little agreement between different studies. Here, we confirm that cordycepin triphosphate is likely to be the active metabolite of cordycepin. Data from single and high throughput experiments showed that cordycepin represses growth factor induced gene expression. Bioinformatic analysis, quantitative PCR and western blotting confirmed that cordycepin blocks the PI3K/AKT/mTOR and/or MEK/ERK pathways in 6 cell lines. Effects of cordycepin on translation through mTOR pathway repression were detectable within 30 minutes, indicating a rapid process. Our data show that cordycepin has a broadly similar mechanism of action in all cell lines studied and indicate that its therapeutic target is a cordycepin triphosphate sensitive molecule that is required for growth factor signal transduction.
2025-02-19 | GSE277620 | GEO
Project description:3’deoxyadenosine, also known as cordycepin, has been widely researched as a potential treatment for cancer, yielding promising results in tissue culture as well as in pre-clinical models. A wide variety of mechanisms of action have been proposed, with little agreement between different studies. Here, we confirm that cordycepin triphosphate is likely to be the active metabolite of cordycepin. Data from single and high throughput experiments showed that cordycepin represses growth factor induced gene expression. Bioinformatic analysis, quantitative PCR and western blotting confirmed that cordycepin blocks the PI3K/AKT/mTOR and/or MEK/ERK pathways in 6 cell lines. Effects of cordycepin on translation through mTOR pathway repression were detectable within 30 minutes, indicating a rapid process. Our data show that cordycepin has a broadly similar mechanism of action in all cell lines studied and indicate that its therapeutic target is a cordycepin triphosphate sensitive molecule that is required for growth factor signal transduction.
2025-02-19 | GSE277557 | GEO
Project description:CD4+ T cells in presence or absence of Ikaros
| PRJNA662885 | ENA
Project description:The aim of the experiment was to gain insight into the selective anti-inflammatory action of the glucocorticoid receptor modulator AZD9567 in comparison with the classical synthetic glucocorticoid dexamethasone. To this end, the transcriptional profile of macrophage RAW 264.7 cells treated with dexamethasone or AZD9567 in the presence or absence of inflammatory response (elicited by lipopolysaccharide treatment) was identified.
2023-06-30 | E-MTAB-12816 | biostudies-arrayexpress
Project description:3’deoxyadenosine, also known as cordycepin, has been widely researched as a potential treatment for cancer, yielding promising results in tissue culture as well as in pre-clinical models. A wide variety of mechanisms of action have been proposed, with little agreement between different studies. Here, we confirm that cordycepin triphosphate is likely to be the active metabolite of cordycepin. Data from single and high throughput experiments showed that cordycepin represses growth factor induced gene expression. Bioinformatic analysis, quantitative PCR and western blotting confirmed that cordycepin blocks the PI3K/AKT/mTOR and/or MEK/ERK pathways in 6 cell lines. Effects of cordycepin on translation through mTOR pathway repression were detectable within 30 minutes, indicating a rapid process. Our data show that cordycepin has a broadly similar mechanism of action in all cell lines studied and indicate that its therapeutic target is a cordycepin triphosphate sensitive molecule that is required for growth factor signal transduction.
2025-02-19 | GSE277825 | GEO