Bcl-2的下调和caspase-8的激活在uvb诱导的人黑色素瘤细胞凋亡中的作用。

K. H. Park, H. Choi, D. Jang, Yong Park, Kyung-Woo Park
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引用次数: 1

摘要

目的:利用体外培养的人黑色素瘤细胞,研究紫外线辐射对细胞凋亡调节蛋白活化的影响。方法:用增加剂量的UVB照射G361浅色素黑色素瘤细胞,通过细胞活力试验、透射电镜(TEM)、流式细胞仪(FACS)和western blotting分析细胞凋亡机制。结果:UVB照射后,TEM和FACS显示细胞死亡的凋亡特征。Western blot结果显示Bcl-2下调,caspase-9激活。Fas/FasL相互作用的下游分子Caspase-8也被激活。caspase-8和caspase-9的下游分子也被激活。结论:我们的数据表明,Bcl-2家族和caspase-8的调控可能共同激活了UVB照射培养的人黑色素瘤细胞后caspase-3介导的凋亡途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Downregulation of Bcl-2 and activation of caspase-8 in the UVB-induced apoptosis of a cultured human melanoma cell line.
Purpose: This study was performed to determine the effect of UV radiation on the activation of apoptosis regulatory proteins using cultured human melanoma cells. Methods: G361 lightly pigmented melanoma cells were irradiated with increasing doses of UVB and analyzed for an apoptotic mechanism using a cell viability test, TEM, FACS, and western blotting analysis. Results: TEM and FACS showed apoptotic features of cell death after UVB irradiation. Western blotting disclosed downregulation of Bcl-2 and the activation of caspase-9. Caspase-8, a downstream molecule of Fas/FasL interaction, was also activated. The activation of downstream molecules of both caspase-8 and caspase-9 was also demonstrated. Conclusion: Our data showed that the regulation of the Bcl-2 family and caspase-8 may work together to activate a caspase-3 mediated apoptotic pathway following UVB irradiation of cultured human melanoma cells.
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