HBXIP upregulates CD46, CD55 and CD59 through ERK1/2/NF-κB signaling to protect breast cancer cells from complement attack
HBXIP upregulates CD46, CD55 and CD59 through ERK1/2/NF-κB signaling to protect breast cancer cells from complement attack
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DOI：
10.1016/j.febslet.2012.01.039
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发表时间：
2012-03-23
期刊：
影响因子：
3.5
通讯作者：
Ye, Lihong
中科院分区：
文献类型：
--
作者：
Cui, Wenjing;Zhao, Yu;Ye, Lihong
Hepatitis B X-interacting protein (HBXIP) is able to enhance migration of breast cancer cells. However, the role of HBXIP in regulation of complement-dependent cytotoxicity (CDC) in breast cancer is not understood. Here, we report that HBXIP contributes to protecting breast cancer cells from CDC by upregulating membrane-bound complement regulatory protein (mCRPs), including CD46, CD55 and CD59. We found that HBXIP upregulated mCRPs through activating p-ERK1/2/NF-kappa B. Interestingly, the knockdown of CD59 was able to block the HBXIP-enhanced breast tumor growth in animal. Thus, we conclude that HBXIP upregulates CD46, CD55 and CD59 through p-ERK1/2/NF-kappa B signaling to protect breast cancer from CDC. Crown Copyright (C) 2012 Published by Elsevier B.V. on behalf of Federation of European Biochemical society. All rights reserved.
