title: [Effect of TAK1 gene silencing on the apoptosis of Kasumi-1 cells induced by arsenic trioxide].
abstract: OBJECTIVE
  To study the effect of transforming growth factor-β activated kinase-1 (TAK1) gene silencing on the proliferation and apoptosis of Kasumi-1 cells induced by arsenic trioxide (As₂O₃).
  
  
  METHODS
  Acute myeloid leukemia with t(8;21) cell line Kasumi-1 cells were treated with As₂O₃ or in combination with TAK1 siRNA interference technology. The experiment was divided into four groups: Kasumi-1 cells without any treatment, TAK1 specific siRNA transfection alone, Kasumi-1 cells treated with different concentration of As₂O₃, TAK1siRNA transfection combined with As₂O₃. CCK-8 was used to detect the cell viability. The expression of phosphorylated c-Jun N-terminal kinase (P-JNK) was determined by Western Blot. Cell apoptosis and growth were examined by morphological and colony formation assay.
  
  
  RESULTS
  After Kasumi-1 cells were treated with As₂O₃, the rate of cell inhibition was concentration-dependent, and the 50% inhibitory concentration was 3.5 μmol/L. The highest expression level of P-JNK appeared in 30 minutes after cells were treated with As₂O₃. The apoptosis rates of Kasumi-1 cells without any treatment, TAK1 siRNA interference alone group, As₂O₃ alone group and the combined group were (5.02 ± 1.13)%, (6.18 ± 0.28)%, (48.33 ± 2.70)% and (86.07 ± 2.21)%; colony formation rates were (73.83 ± 2.78)%, (76.03 ± 1.46)%, (55.07 ± 1.50)% and (22.20 ± 1.15)%; apoptosis rate of TAK1 siRNA group and the untreated group has no significant difference (P = 0.052); colony formation rate between TAk1 siRNA group and the untreated group has no significant difference (P = 0.179), but the difference in other groups was significant (P = 0.000).
  
  
  CONCLUSIONS
  Silencing the expression of TAK1 can enhance the anti-proliferative and pro-apoptotic effect of As₂O₃ on Kasumi-1 cells, and its mechanism may be through the TAK1 downstream JNK signal pathway.
authors.affiliation: Department of Hematology, the Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou 450008, China.
authors.forename: Jin-xia
authors.initials: JX
authors.lastname: Xu
authors.forename: Rui-hua
authors.initials: RH
authors.lastname: Fan
authors.forename: Xu-dong
authors.initials: XD
authors.lastname: Wei
authors.forename: Qing-song
authors.initials: QS
authors.lastname: Yin
authors.forename: Rui-hua
authors.initials: RH
authors.lastname: Mi
authors.forename: Yong-ping
authors.initials: YP
authors.lastname: Song
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D000077237:Arsenic Trioxide; D001152:Arsenicals / Q000494:pharmacology*; D045744:Cell Line, Tumor; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D015470:Leukemia, Myeloid, Acute / Q000201:enzymology / Q000473:pathology*; D020930:MAP Kinase Kinase Kinases / Q000235:genetics* / Q000378:metabolism; D010087:Oxides / Q000494:pharmacology*; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000235:genetics; D015398:Signal Transduction; D000099151:MAP Kinase Kinase Kinase 7
chemical_list: D000077237:Arsenic Trioxide; D001152:Arsenicals; D048031:JNK Mitogen-Activated Protein Kinases; D020930:MAP Kinase Kinase Kinases; D010087:Oxides; D034741:RNA, Small Interfering; D000099151:MAP Kinase Kinase Kinase 7