ArticleMolecular genetics & genomic medicine2019
Sodium butyrate and panobinostat induce apoptosis of chronic myeloid leukemia cells via multiple pathways.
Article in Molecular genetics & genomic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
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- Postbiotics are a candidate for new functional foods.Food chemistry: X · 2024Review
- Histone deacetylase inhibitors for leukemia treatment: current status and future directions.European journal of medical research · 2024Review
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- Epigenetics, Microbiota, and Breast Cancer: A Systematic Review.Life (Basel, Switzerland) · 2024Review
- HDAC inhibitor chidamide overcomes drug resistance in chronic myeloid leukemia with the T315i mutation through the Akt-autophagy pathway.Human cell · 2023Article
- Sodium Butyrate Combined with Docetaxel for the Treatment of Lung Adenocarcinoma A549 Cells by Targeting Gli1.OncoTargets and therapy · 2020Article
- Sodium butyrate and panobinostat induce apoptosis of chronic myeloid leukemia cells via multiple pathways.Molecular genetics & genomic medicine · 2019Article
- Protective autophagy or autophagic death: effects of BEZ235 on chronic myelogenous leukemia.Cancer management and research · 2019Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
purposeHistone deacetylase inhibitor (HDACI) is a novel therapeutic option for cancer. However, the effects of HDACIs on chronic myeloid leukemia (CML) and the underlying mechanisms are still unknown. The aim of this study was to investigate the effect and the mechanism-of-action of two HDACI members, sodium butyrate (NaBu) and panobinostat (LBH589) in K562 and the adriamycin-resistant cell line K562/ADR.
methodsCell viability was assessed using MTT assay. Cell apoptosis was detected with flow cytometry. Cell cycle analysis and western blot were performed to explore the possible molecules related to HDACIs effects.
resultsThe effect of NaBu was more powerful on K562/ADR than on K562 cells. LBH589 triggered apoptosis and inhibited the growth of K562 cells. Both HDACIs inhibited K562 and K562/ADR cells via activation of intrinsic/extrinsic apoptotic pathways and inhibition of AKT-mTOR pathway while NaBu also activated endoplasmic reticulum stress (ERS) mediated apoptotic pathway in K562/ADR cells. LBH589 reduced the expression of drug-resistant related proteins in K562 cells. However, neither NaBu nor LBH589 could significantly influence the expression of the drug-resistant related proteins in K562/ADR cells.
conclusionThe combination of HDACI and other therapeutic strategies are likely required to overcome drug resistance in CML therapy.
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