The anti-cancer effects of cordycepin in MA-10 mouse laydig tumor cells
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PROVIDER: PRJNA448053 | ENA |
REPOSITORIES: ENA
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Project description:Cordycepin, a 3-deoxyadenosine, a traditional Chinese medicine. Studies have demonstrated that cordycepin could modulate multiple signaling pathways to induce cancer cell death. This study aims to determine the genes regulated by Cordycepin and clarify the possible molecular mechanism underlying their action.
2019-05-24 | GSE112513 | GEO
Project description:The purpose of this study was to identify differentially-expressed genes between WT MA-10 mouse tumor Leydig cells and MA-10 cells in which the steroidogenic acute regulatory protein (STAR) is knocked out.
2021-02-11 | GSE165392 | GEO
Project description:To study the potential tumorigenic effect of two activating mutations of hLHR identified in patients, we generated in vitro cell model using mouse Leydig MA-10 cells. The two mutations, Asp578His and Asp578Gly, were stably transfected to MA-10 cell to create MA-10-Asp578His and MA-10-Asp578Gly line. The profile of expressed genes in cells expressing the mutated hLHR was compared with that of control cells using cDNA microarrays with NIA mouse clone sets. Keywords: Genetic modification analysis
2007-03-08 | GSE6780 | GEO
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 (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: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:RNA sequencing of Wild-Type MA-10 cells and STAR Knockout MA-10 cells
| PRJNA694311 | ENA
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:The mitochondrial translocator protein (TSPO) has been shown to bind cholesterol with high affinity and is involved in mediating its availability for steroidogenesis. We recently reported that targeted Tspo gene deletion in MA-10 mouse tumor Leydig cells resulted in reduced cAMP-stimulated steroid formation and significant reduction in the mitochondrial membrane potential (ΔΨm) compared to control cells. We hypothesized that ΔΨm reduction in the absence of TSPO probably reflects the dysregulation and/or maintenance failure of some basic mitochondrial function(s). To explore the consequences of TSPO depletion via CRISPR-Cas9-mediated deletion (indel) mutation in MA-10 cells, we assessed the transcriptome changes in TSPO-mutant versus wild-type (Wt) cells using RNA-seq. Gene expression profiles were validated using real-time PCR. We report herein that there are significant changes in nuclear gene expression in Tspo mutant versus Wt cells. The identified transcriptome changes were mapped to several signaling pathways including the regulation of membrane potential, calcium signaling, extracellular matrix, and phagocytosis. This is a retrograde signaling pathway from the mitochondria to the nucleus and is probably the result of changes in expression of several transcription factors, including key members of the NF-κB pathway. In conclusion, TSPO regulates nuclear gene expression through intracellular signaling. This is the first evidence of a compensatory response to the loss of TSPO with transcriptome changes at the cellular level.
2021-01-09 | GSE164481 | GEO
Project description:The p38 MAPKs play important roles in the regulation of balance between cell survival and cell death on the development of various cancers. However, the roles of p38 MAPKs regulating apoptotic effects on Leydig tumor cells remain unclear. In the present study, we showed that cordycepin (3'-deoxyadenosine) selectively induced apoptosis in MA-10 mouse Leydig tumor cells through regulating the p38 MAPK and PI3K/AKT signaling pathways. Cordycepin reduced viability in MA-10, TM4, and NT2/D1 cells, but not cause cell death of primary mouse Leydig cells on moderate concentration. Cordycepin increased reactive oxygen species (ROS) levels, which is associated with the induction of apoptosis as characterized by positive Annexin V binding, activation of caspase-3, and cleavage of PARP. Inhibition of p38 MAPKs activity by SB203580 significantly prevented cordycepin-induced apoptosis in MA-10 cells. Co-treatment with wortmannin or the autophagy inhibitor 3-methyladenine (3-MA) elevated levels of apoptosis in cordycepin-treated MA-10 cells. Moreover, cordycepin activated p53, p21 and TGFß; and downregulated CDK2. The antitumour activity of cordycepin-treated MA-10 cells was significantly distinct in severe combined immunodeficiency (SCID) mice in vivo. These results suggested that cordycein is a highly selective treatment to induce MA-10 cells apoptosis via p38 MAPKs signaling.
| S-EPMC4548195 | biostudies-literature