ArticleMolecular and cellular biochemistry2010
Inhibition of AMP-activated protein kinase pathway sensitizes human leukemia K562 cells to nontoxic concentration of doxorubicin.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Substituted oxindol-3-ylidenes as AMP-activated protein kinase (AMPK) inhibitors.European journal of medicinal chemistry · 2020Article
- AMP-activated protein kinase α2 and E2F1 transcription factor mediate doxorubicin-induced cytotoxicity by forming a positive signal loop in mouse embryonic fibroblasts and non-carcinoma cells.The Journal of biological chemistry · 2014Article
- BML-275, an AMPK inhibitor, induces DNA damage, G2/M arrest and apoptosis in human pancreatic cancer cells.International journal of oncology · 2012Article
- Alterations of phosphoproteins in NCI-H526 small cell lung cancer cells involved in cytotoxicity of cisplatin and titanocene Y.Neoplasia (New York, N.Y.) · 2012Article
- Effective non-viral delivery of siRNA to acute myeloid leukemia cells with lipid-substituted polyethylenimines.PloS one · 2012Article
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (Dox) is a commonly used anthracycline in many antitumor regimens. The dose related Dox-induced cardiotoxicity often poses challenge in clinical practice, lowering its dose and administering it in combination with other compound is an option. In this study, we found that a nontoxic concentration of Dox at 34.5 nM (20 ng/ml) combined with Compound C, an inhibitor used in AMP-activated protein kinase (AMPK) pathway, could kill human leukemia K562 cells. Additionally, this study confirmed that the combined effect was related to the inhibition of some key proteins such as AMPK and acetyl CoA carboxylase. Moreover, down-regulation of these key proteins in AMPK pathway using siRNA technology also sensitized K562 cells to nontoxic concentration of Dox. The study also showed that Dox at a concentration of 345.0 nM (200 ng/ml) or 862.0 nM (500 ng/ml) that is lower than a typical value of 1-2 microM Dox in patients could kill human leukemia K562 cells. Taken together, our results suggest that inhibition of AMPK pathway by Compound C or siRNA sensitizes K562 cells to nontoxic concentration of Dox which is much lower than typical concentration in plasma of clinical patients.
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