title: [Effect of nuclear transcription factor RelB on the proteasome inhibitor-sensitivity of chronic lymphocytic leukemia cells].
abstract: OBJECTIVE
  To investigate the effect of nuclear transcription factor RelB on the proteasome inhibitor-sensitivity of chronic lymphocytic leukemia (CLL) cells.
  
  
  METHODS
  The mRNA expression of RelB in CD5⁺ CD19⁺ CLL cells from BM was analyzed by reverse transcription PCR (RT-PCR). The RelB activity was examined by electromobility shift assay (EMSA) and an ELISA-based NF-κB family transcription factor activity assay. CLL cells were classified into RelB+ and RelB- groups according to RelB activity. The frequencies of cell death of CLL cells cultured with human bone marrow stromal cells (hBMSCs) after treatment with PS-341, MG-132 or fludarabine were determined by PI staining.
  
  
  RESULTS
  RelB mRNA expression and RelB activity could be detected in CLL cells at variable levels. Fludarabine (10 μmol/L), MG-132 (1 μmol/L) and PS-341 (1 μmol/L) could induce cell death of RelB+ and RelB- CLL cells co-cultured with hBMSCs in a time dependent manner. There was no significant difference in the fludarabine sensitivity between RelB+ and RelB- CLL cells, and the frequencies of cell death of RelB+ and RelB- CLL cells were (61.11 ± 6.91)% and (67.57 ± 9.45)%, respectively, when treated with fludarabine for 72 h. RelB+ CLL cells were more sensitive to MG-132 than RelB- CLL cells for 72 h, and the frequencies of cell death were (66.22 ± 3.39)% and (51.07 ± 5.93)%, respectively. RelB+ CLL cells were more sensitive to PS-341 than RelB- CLL cells for 24 and 48 h treatment, and the frequencies of cell death of RelB+ and RelB- CLL cells were (75.50 ± 4.66)% and (66.32 ± 10.20)% for 24 h, (92.11 ± 3.14)% and (85.84 ± 5.81)% for 48 h treatment, respectively.
  
  
  CONCLUSIONS
  The alternative NF-κB activity was detected in bone marrow derived CLL cells. Enhancement of RelB activity may increase CLL cells' sensitivity to proteasome inhibitor bortezomib and MG-132. However, the sensitivity of CLL cells to fludarabine had no relationship to RelB activity.
authors.affiliation: The Central Laboratory, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
authors.forename: Jingjing
authors.initials: J
authors.lastname: Xu
authors.affiliation: The Central Laboratory, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
authors.forename: Peng
authors.initials: P
authors.lastname: Zhou
authors.affiliation: The Central Laboratory, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
authors.forename: Aining
authors.initials: A
authors.lastname: Sun
authors.affiliation: The Central Laboratory, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Guo
mesh_terms: D016923:Cell Death / Q000187:drug effects; D019008:Drug Resistance, Neoplasm; D006801:Humans; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000378:metabolism / Q000473:pathology*; D016328:NF-kappa B / Q000378:metabolism; D061988:Proteasome Inhibitors / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics; D051841:Transcription Factor RelB / Q000235:genetics / Q000378:metabolism*; D014407:Tumor Cells, Cultured
chemical_list: D016328:NF-kappa B; D061988:Proteasome Inhibitors; C497593:RELB protein, human; D012333:RNA, Messenger; D051841:Transcription Factor RelB