ArticleDrug design, development and therapy2020
Homoharringtonine Exerts an Antimyeloma Effect by Promoting Excess Parkin-Dependent Mitophagy.
Article in Drug design, development and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Homoharringtonine: mechanisms, clinical applications and research progress.Frontiers in oncology · 2025Review
- Ginsenoside Rg1 can restore hematopoietic function by inhibiting Bax translocation-mediated mitochondrial apoptosis in aplastic anemia.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeHomoharringtonine (HHT) has been used as an antileukemia agent in the clinic which processes a high-potential therapeutic efficacy against multiple myeloma (MM). In this study, we investigated the antimyeloma mechanism of HHT.
methodsThree MM cell lines and a xenograft model were applied. Mitochondrial function was evaluated by detecting MitoTracker Green, the mtDNA copy number, mitochondrial protein and enzyme activity, the mitochondrial membrane potential and mitochondrial morphology. Mitophagy levels were assessed by monitoring autophagosomes, performing a colocalization analysis and determining the levels of related proteins. An shRNA was applied to knockdown
resultsBased on the results of the in vitro experiments, HHT exerted a promising antiproliferative effect on the MM.1S, RPMI 8226 and H929 cell lines by increasing mitophagy. In addition, HHT markedly inhibited myeloma tumor growth and prolonged survival by promoting mitophagy in vivo. Furthermore, HHT treatment contributed to notable mitochondrial dysfunction and Parkin-dependent mitophagy, as evidenced by the destruction of mitochondria, the decrease in the mtDNA copy number, decrease in the Bcl-2/Bax ratio, and decrease in the levels of mitochondrial proteins and the optimal expression of Parkin and NDP52. However, the addition of rapamycin did not produce significant synergistic effect with HHT, indicating that HHT reached the threshold level to induce mitophagy. The colocalization analysis and assessment of mitochondrial function examination further confirmed that HHT triggered mitophagy and mitochondrial dysfunction. Moreover, the antiproliferative effect of HHT was reversed by an shRNA targeting
conclusionHHT exerts an antimyeloma effect by inducing excess mitophagy, providing new mechanistic insights into a therapeutic strategy for MM.
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