title: [Enhancive effect of PLK1 gene silencing on sensitivity of K562/A02 cells to adriamycin].
abstract: OBJECTIVE
  Polo-like kinase 1 (PLK1), an important cell cycle regulator, is highly expressed in many types of cancer, and is associated with oncogenesis, treatment effectiveness and prognosis. This study was to investigate the enhancive effect of small interference RNA (siRNA) targeting PLK1 gene on the sensitivity of K562/A02 cells to adriamycin (ADM).
  
  
  METHODS
  siRNA plasmid vector specifically targeting PLK1 gene with enhanced green fluorescent protein (EGFP) was constructed and transfected into K562/A02 cells. The expression of PLK1 was detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. The 50% inhibitory concentration (IC50) of ADM on K562/A02 cells was measured by MTT assay. Intracellular ADM accumulation and ADM-induced apoptosis of K562/A02 cells were detected by flow cytometry.
  
  
  RESULTS
  After treatment with PLK1 siRNA, the mRNA and protein levels of PLK1 in K562/A02 cells were decreased by (61.9+/-2.5)% and (65.3+/-2.4)% of control. The relative reverse rate of sensitivity of K562/A02 cells to ADM was 67.8%. The intracellular accumulation of ADM was greatly increased, and ADM-induced apoptosis of K562/A02 cells was elevated from 11.33% to 54.39%.
  
  
  CONCLUSIONS
  PLK1 gene silencing could enhance intracellular ADM accumulation in K562/A02 cells, improve sensitivity of K562/A02 cells to ADM, and induce cell apoptosis, therefore, reverse cell resistant to ADM.
authors.affiliation: Department of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P. R. China.
authors.forename: Lin
authors.initials: L
authors.lastname: Liu
authors.forename: Min
authors.initials: M
authors.lastname: Zhang
authors.forename: Ping
authors.initials: P
authors.lastname: Zou
authors.forename: Lei
authors.initials: L
authors.lastname: Tian
authors.forename: Fang
authors.initials: F
authors.lastname: Liu
mesh_terms: D000903:Antibiotics, Antineoplastic / Q000378:metabolism / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D018797:Cell Cycle Proteins / Q000096:biosynthesis / Q000235:genetics*; D004317:Doxorubicin / Q000378:metabolism / Q000494:pharmacology*; D019008:Drug Resistance, Neoplasm / Q000187:drug effects*; D015972:Gene Expression Regulation, Neoplastic; D020868:Gene Silencing; D006801:Humans; D020014:K562 Cells / Q000187:drug effects / Q000473:pathology; D017346:Protein Serine-Threonine Kinases / Q000096:biosynthesis / Q000235:genetics*; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis / Q000235:genetics*; D012333:RNA, Messenger / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics*; D014162:Transfection; D000097869:Polo-Like Kinase 1
chemical_list: D000903:Antibiotics, Antineoplastic; D018797:Cell Cycle Proteins; D004317:Doxorubicin; D017346:Protein Serine-Threonine Kinases; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D000097869:Polo-Like Kinase 1