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首页> 外文期刊>Molecular and Cellular Biology >NF-κB Induces Expression of the Bcl-2 Homologue A1/Bfl-1 To Preferentially Suppress Chemotherapy-Induced Apoptosis
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NF-κB Induces Expression of the Bcl-2 Homologue A1/Bfl-1 To Preferentially Suppress Chemotherapy-Induced Apoptosis

机译：NF-κB诱导Bcl-2同源物A1 / Bfl-1的表达，以优先抑制化疗诱导的细胞凋亡。

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Recent evidence indicates that the transcription factor NF-κB is a major effector of inducible antiapoptotic mechanisms. For example, it was shown that NF-κB activation suppresses the activation of caspase 8, the apical caspase in tumor necrosis factor (TNF) receptor family signaling cascades, through the transcriptional regulation of certain TRAF and IAP proteins. However, it was unknown whether NF-κB controls other key regulatory mechanisms in apoptosis. Here we show that NF-κB activation suppresses mitochondrial release of cytochrome cthrough the activation of the Bcl-2 family member A1/Bfl-1. The restoration of A1 in NF-κB null cells diminished TNF-induced apoptosis by reducing the release of proapoptotic cytochromec from mitochondria. In addition, A1 potently inhibited etoposide-induced apoptosis by inhibiting the release of cytochromec and by blocking caspase 3 activation. Our findings demonstrate that A1 is an important antiapoptotic gene controlled by NF-κB and establish that the prosurvival function of NF-κB can be manifested at multiple levels.
机译：最近的证据表明，转录因子NF-κB是诱导型抗凋亡机制的主要效应器。例如，已显示NF-κB激活通过某些TRAF和IAP蛋白的转录调控抑制了胱天蛋白酶8的激活，胱天蛋白酶8是肿瘤坏死因子（TNF）受体家族信号级联反应中的顶端胱天蛋白酶。但是，尚不清楚NF-κB是否控制凋亡中的其他关键调控机制。在这里，我们显示NF-κB激活通过Bcl-2家族成员A1 / Bfl-1的激活抑制线粒体细胞色素 c 的释放。通过减少线粒体促凋亡细胞色素 c 的释放，NF-κB无效细胞中A1的恢复减少了TNF诱导的细胞凋亡。此外，A1通过抑制细胞色素 c 的释放和阻断caspase 3的激活来有效抑制依托泊苷诱导的细胞凋亡。我们的发现表明，A1是由NF-κB控制的重要抗凋亡基因，并确定NF-κB的生存功能可以在多个水平上体现。

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