The effection of celastrol treatment on SKM-1 cell
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PROVIDER: PRJNA1158269 | ENA |
REPOSITORIES: ENA
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Project description:Myelodysplastic syndromes (MDS) are myeloid hematopoietic stem cell tumors displaying complex pathogenesis with a high risk of transformation to acute myeloid leukemia (AML). The efficacy of current clinical drugs is limited. Thus, identifying high-efficiency drugs of MDS remain urgent. Celastrol, a natural small molecule compound derived from the traditional Chinese medicinal herb Tripterygium wilfordii, has shown powerful antitumor effects. However, the effects of celastrol on MDS are unknown. In this study, we found that celastrol significantly inhibited the viability of MDS cell lines and bone marrow mononuclear cells (BMMCs) from MDS patients, and induced apoptosis. Through transcriptome sequencing, we found that celastrol induced the pro-apoptotic ER stress response in MDS cell. Mechanistically, celastrol activated the pro-apoptotic ER-stress branch involving the pancreatic eIF2α kinase (PERK) pathway.
2025-09-06 | GSE276645 | GEO
Project description:Celastrol has been shown to sensitize leptin receptor signaling and reduce ER stress. Current microarray data provide the gene expression profile in mouse embryonic fibroblasts (MEFs) after Celastrol treatment compared with control.
2016-07-08 | GSE84154 | GEO
Project description:To profile the global effects of Commd3 deficiency on humoral immune responses, CD45+ cells from the draining lymph nodes (LNs) of CreERT2Commd3flox/+ and CreERT2Commd3flox/flox mice were subjected to single-cell RNA sequencing (scRNA-seq) at 7 days after immunization. We found that Commd3 deletion a week before immunization reduced only the proportion of germinal center B cells with minimal transcriptomic changes in B cell populations. Celastrol treatment in WT mice a week before immunization also selectively reduced the proportion of GC B cells with little impact on the transcriptomes, whereas none of the detectable immune cell populations were significantly affected by celastrol treatment in the immunized COMMD3C170A/C170A mice.
2023-03-31 | GSE197580 | GEO
Project description:RNA-seq upon Celastrol (200 nM) treatment in the neuroblastoma cell line CLB-GA. Analysis was performed 48h upon treatment. Four biological replicates per condition.
2021-07-01 | E-MTAB-9315 | biostudies-arrayexpress
Project description:Celastrol is a natural product that affects LNCaP gene expression by 6h We used microarrays to detail the global programme of gene expression affected by celastrol treatment at 6h Keywords: drug treatment
2006-09-01 | GSE5505 | GEO
Project description:Celastrol is a natural product that affects LNCaP gene expression by 6h; We used microarrays to detail the global programme of gene expression affected by celastrol treatment at 6h Experiment Overall Design: LNCaP cells were grown to 50% confluency and treated with celastrol for 6h prior to direct Trizol lysis and RNA isolation
2008-11-07 | E-GEOD-5505 | biostudies-arrayexpress
Project description:Stress response pathways allow cells to rapidly sense and respond to deleterious environmental changes, including those caused by pathophysiological disease states. A previous screen for small molecules capable of activating the human heat shock response identified the triterpenoid celastrol as a potent activator of the heat shock transcription factor HSF1. We show here that celastrol likewise activates the homologous Hsf1 of Saccharomyces cerevisiae. Celastrol induced Hsf1 hyperphosphorylation and concurrently activated a synthetic transcriptional reporter as well as endogenous inducible Hsp70 proteins at the same effective concentration seen in mammalian cells. Moreover, celastrol treatment conferred significant resistance to subsequent lethal heat shock. Transcriptional profiling experiments revealed that in addition to Hsf1, celastrol treatment induced the Yap1-dependent oxidant defense regulon. Oxidative stress-responsive genes were likewise induced in mammalian cells, demonstrating that celastrol simultaneously activates two major cellular stress-mediating pathways. As the induction of cellular stress pathways has implications in the treatment of a variety of human diseases including neurodegenerative diosorders, cardiovascular disease and cancer, celastrol thus represents an attractive therapeutic compound. Keywords: single-dose, single time-point gene induction by natural small molecule celastrol compared to heat shock in wild type (BY4741) Saccahromyces cerevisiae
2006-08-26 | GSE5608 | GEO
Project description:celastrol is a natural product that affects LNCaP androgen-signalling by 24h We used microarrays to detail the androgen-responsive program of gene expression affected by celastrol treatment at 24h Keywords: drug treatment
2006-09-01 | GSE5507 | GEO
Project description:celastrol is a natural product that affects LNCaP androgen-signalling by 24h; We used microarrays to detail the androgen-responsive program of gene expression affected by celastrol treatment at 24h Experiment Overall Design: LNCaP cells were grown to 50% confluency and deprived of androgen, and subsequently treated with celastrol plus androgen, androgen alone, or vehicle alone for 24h prior to direct Trizol lysis and RNA isolation
2008-11-07 | E-GEOD-5507 | biostudies-arrayexpress
Project description:Purpose: The goals of this study was to (1) evaluate the protective effect of celastrol on alpha-naphthylisothiocyanate (ANIT)-induced cholestasis and (2) which genes were recovered by celastrol. Methods:To investigate the protective effect of celastrol on ANIT-induced cholestasis, the WT mice were randomly assigned into two groups, respectively (n=3): (1) ANIT; (2) ANIT+Celastrol. ANIT+Celastrol group was orally treated with celastrol (10 mg/kg dissolved in 1% DMSO + 2% Tween 80 + 97% water) for 5 consecutive days. After celastrol was treated for 3 days, ANIT and ANIT+Celastrol groups were given a single oral dose of ANIT. All mice were killed 48 h after ANIT administration. Liver samples were harvested and frozen at -80 °C before analysis. Results: A total of 978 DEGs were identified. Large numbers of these DEGs were related to activation of SIRT1, which included increased FXR signaling and inhibition of PPARγ, nuclear factor-kappa B (NF-κB), and P53 signaling. Conclusions: Celastrol could protect ANIT-induced cholestasis by recovering disrupted Sirt1 level.
2018-02-09 | GSE110391 | GEO