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HBXIP upregulates CD46, CD55 and CD59 through ERK1/2/NF‐κB signaling to protect breast cancer cells from complement attack
Author(s) -
Cui Wenjing,
Zhao Yu,
Shan Changliang,
Kong Guangyao,
Hu Nan,
Zhang Yiwen,
Zhang Shuai,
Zhang Weiying,
Zhang Yingyi,
Zhang Xiaodong,
Ye Lihong
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.01.039
Subject(s) - cd59 , complement dependent cytotoxicity , downregulation and upregulation , cancer research , breast cancer , gene knockdown , cd46 , nf κb , cytotoxicity , chemistry , cancer , signal transduction , biology , complement system , immunology , medicine , microbiology and biotechnology , immune system , apoptosis , biochemistry , gene , antibody dependent cell mediated cytotoxicity , in vitro
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‐κB. 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‐κB signaling to protect breast cancer from CDC.