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  • Title: [The modulating effect of proapoptotic protein Bax on the resistance of malignant lymphoma cells to tumor necrosis factor related apoptosis inducing ligand-induced apoptosis].
    Author: Hao JH, Yu M, Jia L, Liu FT, Li Q, Hao XS.
    Journal: Zhonghua Yi Xue Za Zhi; 2007 Jan 09; 87(2):134-7. PubMed ID: 17418025.
    Abstract:
    OBJECTIVE: To elucidate the modulating effect of proapoptotic protein Bax on the resistance of malignant lymphoma cells to tumor necrotic factor-related apoptosis inducing ligand (TRAIL)-induced apoptosis and offer evidence for clinic work. METHODS: Human malignant lymphoma cells of the line CRL and normal HRC cells were cultured and treated by 500 g/L TRAIL (Group T), treated by 10 nmol/L PS-341 (Group P), or pre-treated by 10 nmol/L proteasome inhibitor PS-341 for 1 hour and then treated by 500 microg/L TRAIL (Group P + T). Flow cytometry was used to detect the cell apoptosis. Western blotting was used to detect the expression of Bax protein. Caspase-8 activity was tested by fluorophotometer. Immunoprecipitation method was used to examine the conformation change of Bax protein. RESULTS: The apoptosis index 24 hours after treatment of the CRL cells of Group T was 21%, significantly lower than that of the HRC cells of Group T (32%, P < 0.01). The Bax protein expression amount 24 hours after treatment of the HRC cells of Group T was 1.8 times that of the normal cells, and the Bax protein expression amount 24 hours after treatment of the CRL cells of Group T was only 5/17 that of the normal amount. The apoptotic index 6 hours after treatment of the CRL cells of Group P + T was 54%, significantly higher than those of Groups T and P (both P < 0.01). The caspase-8 activity 6 hours after treatment of the CRL cells of Group P + T was 26.5 micromol.L(-1).h(-1).mg(-1) protein, similar to that of the HRC cells of Group P + T (27.2 micromol.L(-1).h(-1).mg(-1) protein), and significantly higher than those of the other cells (all P < 0.01). The Bax protein expression 6 hours after treatment of the Group P HRC and CRL cells were 2.5 times and 1.2 times that of the control cells. The Bax protein expression of the HRC cells of Group P + T was 3.3 times that of the normal controls, and the Bax degradation of the CRL cells of Group P + T was significantly reduced. The combination treatment of P + T significantly increased the expression of activated Bax. CONCLUSION: Bax degradation plays an important role in the resistance of malignant lymphoma to TRAIL-induced apoptosis. Using proteasome inhibitor can inhibit the protein degradation and overcome the drug resistance.
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