title: [In vitro killing effects of STI571 on esophageal carcinoma cell lines CE-48T and CE-81T].
abstract: OBJECTIVE
  Tyrosine kinase mediates cell proliferation and differentiation, and plays important roles in tumorigenesis and development of esophageal carcinoma. STI571 is a tyrosine kinase inhibitor of platelet-derived growth factor receptor beta (PDGFR-beta) which is overexpressed in esophageal carcinoma. This study was to explore the in vitro killing effects of STI571 on esophageal carcinoma cell lines CE-48T and CE-81T.
  
  
  METHODS
  The expression of PDGFR-alpha and PDGFR-beta in CE-48T and CE-81T cells was detected by Western blot. The killing effects of STI571 on CE-48T and CE-81T cells were evaluated by MTT assay. Cell apoptosis was analyzed by flow cytometry with Annexin V/PI labeling. The expression of p-PDGFR-beta was detected by Western blot before and after treatment of STI571.
  
  
  RESULTS
  CE-48T cells expressed PDGFR-beta, but did not express PDGFR-alpha; CE-81T cells did not express both PDGFR-alpha and PDGFR-beta. The 50% inhibitory concentration (IC50) of STI571 was significantly lower for CE-48T cells than for CE-81T cells [(8.32+/-1.50) micromol/L vs. (41.02+/-7.64) micromol/L, P=0.002]. When treated with 10 micromol/L STI571 for 12 h, the apoptosis rate of CE-48T cells was (52.43+/-5.30)%, but the apoptosis rate did not increase as the treatment time and concentration increased. After treatment of STI571, the expression of p-PDGFR-beta was inhibited in CE-48T cells, but didn't change in CE-81T cells.
  
  
  CONCLUSIONS
  STI-571 could induce the apoptosis of PDGFR-beta-positive esophageal carcinoma CE-48T cells. p-PDGFR-beta might be the target of STI571.
authors.affiliation: State Key Laboratory of Oncology in South China, Guangzhou, Guangdong 510060, China.
authors.forename: Peng-Yuan
authors.initials: PY
authors.lastname: Zhang
authors.forename: Bao-Jiang
authors.initials: BJ
authors.lastname: Li
authors.forename: Xiao-Dong
authors.initials: XD
authors.lastname: Su
authors.forename: Zhe-Sheng
authors.initials: ZS
authors.lastname: Wen
authors.forename: Jin-Ming
authors.initials: JM
authors.lastname: Zhao
authors.forename: Lan-Jun
authors.initials: LJ
authors.lastname: Zhang
authors.forename: Hao
authors.initials: H
authors.lastname: Long
authors.forename: Tie-Hua
authors.initials: TH
authors.lastname: Rong
mesh_terms: D000970:Antineoplastic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D001549:Benzamides; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D016503:Drug Delivery Systems; D004938:Esophageal Neoplasms / Q000473:pathology*; D006801:Humans; D000068877:Imatinib Mesylate; D010879:Piperazines / Q000008:administration & dosage / Q000494:pharmacology*; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors; D011743:Pyrimidines / Q000008:administration & dosage / Q000494:pharmacology*; D020796:Receptor, Platelet-Derived Growth Factor alpha / Q000378:metabolism; D020797:Receptor, Platelet-Derived Growth Factor beta / Q000378:metabolism*
chemical_list: D000970:Antineoplastic Agents; D001549:Benzamides; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D011505:Protein-Tyrosine Kinases; D020796:Receptor, Platelet-Derived Growth Factor alpha; D020797:Receptor, Platelet-Derived Growth Factor beta