Bcl-3, induced by Tax and HTLV-1, inhibits NF-¦ÊB activation and promotes autophagy

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• 作者：Jinheng Wang ; Zhiguo Niu ; Ying Shi ; Cai Gao ; Xia Wang ; Jingxian Han ; Junying Li ; Zhitao Gao ; Xiaofei Zhu ; Xiangfeng Song ; Zhihai Qin ; Hui Wang
• 关键词：HTLV-1 ; Tax ; Bcl-3 ; NF-¦ÊB activation ; Autophagy
• 刊名：Cellular Signalling
• 出版年：2013
• 出版时间：December, 2013
• 年：2013
• 卷：25
• 期：12
• 页码：2797-2804
• 全文大小：1271 K

文摘

The human T cell leukemia virus type 1 (HTLV-1) is a complex human retrovirus that causes an aggressive leukemia known as adult T cell leukemia (ATL). The HTLV-1-encoded oncoprotein Tax induces persistent activation of the nuclear factor-¦ÊB (NF-¦ÊB) pathway, which is perceived as the primary cause of ATL. Bcl-3, a member of the NF-¦ÊB inhibitor (I¦ÊB) family, is highly expressed in many HTLV-1-infected T cell lines and ATL cells. However, the role of Bcl-3 in Tax-induced NF-¦ÊB activation has not been fully elucidated. Here, we show that Tax induces Bcl-3 expression, which in turn negatively regulates the Tax-induced NF-¦ÊB activation. Interestingly, both Bcl-3 up-regulation and NF-¦ÊB inhibition promote the autophagy process in HTLV-1-infected cells. Consistent with this, over-expression of Bcl-3 also results in enhancement of rapamycin-, pifithrin-¦Á- or starvation-induced autophagy in control cells. Together, these data demonstrate that Bcl-3 acts as a negative regulator of NF-¦ÊB activation and promotes autophagy in HTLV-1-infected cells.