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The effection of celastrol treatment on SKM-1 cell

GSE276645 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/09/06 Platform GPL34284
Summary
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.
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Direct links to NCBI, no account and no request form: the whole study as GSE276645_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 6 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1158269 and SRA study SRP531307. Searching any of these in the dataset finder brings you back here.

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