Inhibition of NF-kappa B can enhance Fas-mediated apoptosis in leukemia cell line HL-60

被引:10
作者
Wang L. [1 ]
Zhao S. [1 ,2 ]
Wang H.-X. [1 ]
Zou P. [2 ]
机构
[1] Department of Hematology, The Central Hospital of Wuhan
[2] Department of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology
来源
Frontiers of Medicine in China | 2010年 / 4卷 / 3期
关键词
Bay; 11-7082; Fas/FasL system; HL-60; nuclear factor-kappa B;
D O I
10.1007/s11684-010-0026-5
中图分类号
学科分类号
摘要
This study explored the effects of nuclear factor-kappa B (NF-κB) inhibitor Bay 11-7082 on Fas/FasL system and Fas-mediated apoptosis in cell line HL-60 cells. The mRNA and protein levels of Fas, FasL, and X-linked inhibitor of apoptosis protein (XIAP) were detected by reverse transcription-polymerase chain reaction (RT-PCR) and flow cytometry (FCM); the level of sFasL was evaluated by enzyme-linked immunosorbent assay (ELISA); and apoptosis was determined by FCM. After treatment with Bay 11-7082, the mRNA and protein levels of FasL and XIAP in HL-60 cells were significantly lower than in the controls (P < 0.05), but the mRNA and protein levels of Fas and sFasL did not change significantly (P > 0.05). Apoptotic rate of HL-60 cells treated with Bay 11-7082 was significantly higher than in the controls (P < 0.05). Therefore, we conclude that Bay 11-7082 can enhance Fas-mediated apoptosis in HL-60 cells by downregulating FasL and XIAP levels. © 2010 Higher Education Press and Springer-Verlag Berlin Heidelberg.
引用
收藏
页码:323 / 328
页数:5
相关论文
共 23 条
[1]
Friesen C., Herr I., Krammer P.H., Debatin K.M., Involvement of the CD95(APO-1/Fas)receptor/ligand system in drug-induced apoptosis in leukaemia cell, Nature Med, 2, 5, pp. 574-577, (1996)
[2]
Kim K.M., Lee K., Hong Y.S., Park H.Y., Fas-mediated apoptosis and expression of related genes in human malignant hematopoietic cell, Exp Mol Med, 32, 4, pp. 246-254, (2000)
[3]
Kordes U., Krappmann D., Heissmeyer V., Ludwig W.D., Scheidereit C., Transcription factor NF-κB is constitutively activated in acute lymphoblastic leukemia cells, Leukemia, 14, 3, pp. 399-402, (2000)
[4]
Qin Y., Camoretti-Mercado B., Blokh L., Long C.G., Ko F.D., Hamann K.J., Fas Resistance of Leukemic Eosinophils Is Due to Activation of NF-κB by Fas Ligation, J Immunol, 169, 7, pp. 3536-3544, (2002)
[5]
Bueso-Ramos C.E., Rocha F.C., Shishodia S., Medeiros L.J., Kantarjian H.M., Vadhan-Raj S., Estrov Z., Smith T.L., Nguyen M.H., Aggarwal B.B., Expression of constitutively active nuclear-kappa B RelA transcription factor in blasts of acute myeloid leukemia, Hum Pathol, 35, 2, pp. 246-253, (2004)
[6]
Hafez M., Al-Tonbary Y., El-Bayoumi M.A., Hatem N., Hawas S., Mansour A., Marzouk I., Hafez M.M., Yahia S., Farahat N., Markers of apoptosis and proliferation related gene products as predictors of treatment outcome in childhood acute lymphoblastic leukemia, Hematology, 12, 3, pp. 209-218, (2007)
[7]
Qin Y., Camoretti-Mercado B., Blokh L., Long C.G., Ko F.D., Hamann K.J., Fas Resistance of Leukemic Eosinophils Is Due to Activation of NF-κB by Fas Ligation, J Immunol, 169, 7, pp. 3536-3544, (2002)
[8]
Barnhart B.C., Pietras E.M., Algeciras-Schimnich A., Salmena L., Sayama K., Hakem R., Peter M.E., CD95 apoptosis resistance in certain cells can be overcome by noncanonical activation of caspase-8, Cell Death Differ, 12, 1, pp. 25-37, (2005)
[9]
Meli M., D'Alessandro N., Tolomeo M., Rausa L., Notarbartolo M., Dusonchet L., NF-κB Inhibiton Restores Sensitivity to Fas-Mediated Apoptosis in Lymphoma Cell Lines, Ann N Y Acad Sci, 1010, pp. 232-236, (2003)
[10]
Buzyn A., Petit F., Ostankovitch M., Figueiredo S., Varet B., Guillet J.G., Ameisen J.C., Estaquier J., Membrane-bound Fas ligand on leukemic cells: A mechanism of tumor immune escape in leukemic patients, Blood, 94, 9, pp. 3135-3140, (1999)