Acadesine Inhibits the Proliferation of K562 Cells and Enhances their Sensitivity to Imatinib.
- Author:
Jing-Jing WU
1
;
Bin WEI
1
;
Yi-Han DING
1
;
Zhi-Kui DENG
1
;
Yu-Ye SHI
1
;
Yu-Feng LI
2
Author Information
- Publication Type:Journal Article
- MeSH: Aminoimidazole Carboxamide; analogs & derivatives; pharmacology; Apoptosis; Caspase 3; metabolism; Cell Cycle Checkpoints; Cell Proliferation; drug effects; Cyclin D1; metabolism; Cyclin E; metabolism; Humans; Imatinib Mesylate; pharmacology; K562 Cells; drug effects; Oncogene Proteins; metabolism; Ribonucleosides; pharmacology
- From: Journal of Experimental Hematology 2016;24(1):36-40
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of AMPK agonist Acadesine (AICAR) on growth inhibition of K562 cells and their sensitivity to imatinib (IM).
METHODSK562 cells were cultured with different concentrations of AICAR alone or its combination with IM for 48 hours, the CCK-8 assay was used to detect cell proliferation, the cell cycle distribution and apoptosis were analyzed by flow cytometry. The expression levels of Cyclin D1, Cyclin E1 and Caspase 3 protein were determined by Western blot.
RESULTSAICAR inhibited the proliferation of K562 cells in dose-dependent manner, and their IC50 value was 0.45 mmol/L at 48 hours. AICAR could induce arrest of K562 cells in G1 phase and down-regulated the protein expression levels of Cyclin D1 and Cyclin E1; whereas it didn't influence the cell apoptosis. Additionally, the growth inhibition of cells induced by IM was enhanced by AICAR.
CONCLUSIONAICAR can inhibit the proliferation of K562 cells by arresting the cell cycle and enhancing the sensitivity of K562 cells to IM.
