title: [Effect of A Novel Emodin Derivative on Chronic Myelogenous Leukemia K562 Cells and Imatinib-resistant K562/G01 Cells].
abstract: OBJECTIVE
  To explore the effect of a novel emodin derivative E19 on proliferation inhibition and apoptosis induction of human chronic myelogenous leukemia (CML) cell line K562 and imatinib-resistant CML cell line (K562/G01), and to clarify the involved mechanisms.
  
  
  METHODS
  MTT and colony formation test were used to detect the cell proliferation. Apoptotic induction effects were examined by DAPI staining method and DNA ladder assay. Western blot was performed to detect the changes of P210(Bcr-Abl) protein.
  
  
  RESULTS
  The emodin derivative E19 could efficiently inhibit proliferation and induce apoptosis in K562 and K562/G01 cells. IC50 of K562 cells and IC50 of K562/G01 cells were (1.20 ± 0.19) µmol/L and (1.22 ± 0.16) µmol/L, respectively. DNA fragmentation in K562 cells and K562/G01 cells confirmed that the E19 induced apoptosis in dose-dependent manner. Western blot showed that emodin derivative inhibited phosphorylation of P210 protein in K562 cells and K562/G01 cells and down-regulated the expression level of P210 in dose- and time-dependent manners.
  
  
  CONCLUSIONS
  The emodin derivative E19 can efficiently inhibit growth and induce apoptosis of K562 cells and K562/G01 cells, while the inhibition of phosphorylation of P210 protein and down-regulation of P210 protein expression may be involved in these processes.
authors.affiliation: Fujian Institute of Hematology, Fujian Medical University Union Hospital, Fuzhou 350001, Fujian Province, China.|Department of Hematology, People's Hospital, Affiliated to Hubei University of Medicine, Shiyan 442000, Hubei Province, China.
authors.forename: Bo-Jun
authors.initials: BJ
authors.lastname: Li
authors.affiliation: Fujian Institute of Hematology, Fujian Medical University Union Hospital, Fuzhou 350001, Fujian Province, China.
authors.forename: Ting-Bo
authors.initials: TB
authors.lastname: Liu
authors.affiliation: School of Chemistry and Chemical Engineering, Fuzhou University, Fuzhou 350108, Fujian Province, China.
authors.forename: Wen-Feng
authors.initials: WF
authors.lastname: Wang
authors.affiliation: Fujian Institute of Hematology, Fujian Medical University Union Hospital, Fuzhou 350001, Fujian Province, China.
authors.forename: Min-Hui
authors.initials: MH
authors.lastname: Lin
authors.affiliation: Fujian Institute of Hematology, Fujian Medical University Union Hospital, Fuzhou 350001, Fujian Province, China. E-mail: jdhu@medmail.com.cn.
authors.forename: Jian-Da
authors.initials: JD
authors.lastname: Hu
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D049109:Cell Proliferation; D015536:Down-Regulation; D019008:Drug Resistance, Neoplasm; D004642:Emodin / Q000031:analogs & derivatives / Q000494:pharmacology*; D016044:Fusion Proteins, bcr-abl / Q000378:metabolism; D006801:Humans; D000068877:Imatinib Mesylate / Q000494:pharmacology; D020014:K562 Cells / Q000187:drug effects; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000473:pathology*; D010766:Phosphorylation
chemical_list: D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl; D004642:Emodin