title: [Effect of Arsenic Trioxide on K562 Cell Proliferation and Its Mechanism].
abstract: OBJECTIVE
  To investigate the molecular mechanism of arsenic trioxide(ATO) inhibiting K562 cell proliferation, and explore the new targets for treating chronic myeloid leukemia(CML).
  
  
  METHODS
  human CML cell line K562 cells were cultured in vitro, and were treated with different concentrations of ATO; MTT was used to detect the cell proliferation; flow cytometry(FCM) was used to determine cell apoptosis, cell cycle and the expression of CD44; Transcriptional levels of β-catenin and cyclin D1 were assayed by RT-PCR.
  
  
  RESULTS
  2 µmol/L ATO could inhibit the cell proliferation obviously in a time-and-dose-dependent manner. With drug concentration increasing and time prolonging, the expression rate of CD44 was declined gradrually. FCM with AnnexinV/PI double staining showed that K562 cells were induced to apoptosis after exposure to 2.5-10 µmol/L ATO for 48 hours and in dose-dependent manner. Treating with different concentration ATO for 48 hours, cell ratio of G0/G1phase increased and cell ratio in S phase decreased gradually. RT-PCR showed that the expression of β-catenin and CyclinD1 decreased with increasing of drug concentration.
  
  
  CONCLUSIONS
  ATO in certain concentration range can inhibit K562 cell proliferation, and induce the cell apotosis, the mechanismin influencing the Wnt/β-catenin pathway may be the downregulation of CD44 expression, arresting K562 cells in G0/G1phase, and affecting the gene transcription, thus inhibiting K562 cell proliferation.
authors.affiliation: Department of Hematology, Hebei Provincial People's Hospital, Shijiazhuang 050051, Hebei Province, China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Hematology, Hebei Provincial People's Hospital, Shijiazhuang 050051, Hebei Province, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Yang
authors.affiliation: Department of Hematology, Hebei Provincial People's Hospital, Shijiazhuang 050051, Hebei Province, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Li
authors.affiliation: Department of Hematology, Hebei Provincial People's Hospital, Shijiazhuang 050051, Hebei Province, China.
authors.forename: Rui-Cang
authors.initials: RC
authors.lastname: Wang
authors.affiliation: Department of Hematology, Hebei Provincial People's Hospital, Shijiazhuang 050051, Hebei Province, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Yuan
authors.affiliation: Department of Hematology, Hebei Provincial People's Hospital, Shijiazhuang 050051, Hebei Province, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Hematology, Hebei Provincial People's Hospital, Shijiazhuang 050051, Hebei Province, China.
authors.forename: Su-Yun
authors.initials: SY
authors.lastname: Wang
authors.affiliation: Department of Hematology, Hebei Provincial People's Hospital, Shijiazhuang 050051, Hebei Province, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Wang
authors.affiliation: Department of Hematology, Hebei Provincial People's Hospital, Shijiazhuang 050051, Hebei Province, China. E-mail: h0707@163.com.
authors.forename: Hong-Ling
authors.initials: HL
authors.lastname: Hao
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D000077237:Arsenic Trioxide; D001152:Arsenicals / Q000494:pharmacology*; D002453:Cell Cycle; D049109:Cell Proliferation / Q000187:drug effects*; D006801:Humans; D020014:K562 Cells; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy*; D010087:Oxides / Q000494:pharmacology*
chemical_list: D000970:Antineoplastic Agents; D001152:Arsenicals; D010087:Oxides; D000077237:Arsenic Trioxide