ArticleTranslational cancer research2025
Demethylzeylasteral alleviates myeloid leukemia through PERK/eIF2α/ATF4/CHOP-mediated cell apoptosis.
Article in Translational cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Myeloid leukemia, as a malignant tumor of hematologic system, urgently requires discovery of novel therapeutic drugs. Demethylzeylasteral (DML), a natural terpenoid primary extract from Tripterygium, has demonstrated antitumor properties across various cancer types. However, its functions in myeloid leukemia have not been clearly elucidated. This study aimed to explore the effects of DML on the proliferation and apoptosis of myeloid leukemia cells, and elucidate its mechanism. Methods: Cell viability was detected by Cell Count Kit-8 (CCK-8) method. Post-DML treatment, cell cycle, apoptosis, intensity of unfolded proteins, adenosine triphosphate (ATP), intracellular calcium, and reactive oxygen species (ROS) levels were assessed by flow cytometry. Additionally, transcriptome sequencing and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were conducted to uncover pathways linked to gene enrichment in the DML treatment group, which were validated using small molecular inhibitors, short hairpin RNA (shRNA) interference, flow cytometry, reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis. Results: A library of 65 terpenoids was screened against myeloid leukemia cell lines (K562, NB4, THP-1), identifying DML through screening and validation using CCK-8 assays. Comprehensive Conclusions: These results systematically establish that DML induces apoptosis in myeloid leukemia cells directly through PERK/eIF2α/ATF4/CHOP signaling pathway in response to ER stress.
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