- Author:
Wei LI
1
;
Ying ZHAO
;
Bo TAO
;
Ying ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Cell Cycle; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Cell Survival; drug effects; Fusion Proteins, bcr-abl; genetics; metabolism; Gene Expression Regulation, Leukemic; drug effects; Hedgehog Proteins; metabolism; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; genetics; pathology; Quercetin; pharmacology; RNA, Messenger; genetics; metabolism; Signal Transduction; drug effects
- From: Chinese journal of integrative medicine 2014;20(10):776-781
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the effects of quercetin on Hedgehog (Hh) signaling in chronic myeloid leukemia KBM7 cells.
METHODSThe KBM7 cells were treated with 50, 100 and 200 μmol/L quercetin for 48 h respectively. And then the trypan blue assay was used to examine the proliferative inhibition of quercetin. Apoptotic cells and cell cycle were measured by flow cytometry. The mRNA and protein expression were detected by quantitative real-time polymerase chain reaction (PCR) and Western blot, respectively.
RESULTSQuercetin significantly inhibited KBM7 cell proliferation, induced cell apoptosis, and blocked cell cycle at G1 phase, which were in dose-dependent manners. The mRNA and protein expression of Smoothened and Glioma1 (Gli1), the members of Hh pathway decreased after treatment with quercetin. The Bcl-2 and Cyclin D1, targets of Hh signaling, also decreased after treatment with quercetin, respectively. Quercetin also could increase p53 and Caspase-3 expression. Bcr-abl mRNA copies decreased, but no changes of phosphorylated Bcr-abl and Bcr-abl proteins were observed, after treatment with quercetin.
CONCLUSIONQuercetin could inhibit Hh signaling and its downstream targets in the KBM7 cells. And it might be one of mechanisms of inducing apoptosis and inhibiting cell cycle by quercetin.