HBXIP upregulates CD46, CD55 and CD59 through ERK1/2/NF-κB signaling to protect breast cancer cells from complement attack

Wenjing Cui; Yu Zhao; Changliang Shan; Guangyao Kong; Nan Hu; Yiwen Zhang; Shuai Zhang; Weiying Zhang; Yingyi Zhang; Xiaodong Zhang; Lihong Ye

doi:10.1016/j.febslet.2012.01.039

HBXIP upregulates CD46, CD55 and CD59 through ERK1/2/NF-κB signaling to protect breast cancer cells from complement attack

Wenjing Cui
, Yu Zhao
, Changliang Shan
, Guangyao Kong
, Nan Hu
, Yiwen Zhang
, Shuai Zhang
, Weiying Zhang
, Yingyi Zhang
, Xiaodong Zhang
, Lihong Ye

Nankai University

Research output: Contribution to journal › Article › peer-review

44 Scopus citations

Abstract

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. Crown

Original language	English
Pages (from-to)	766-771
Number of pages	6
Journal	FEBS Letters
Volume	586
Issue number	6
DOIs	https://doi.org/10.1016/j.febslet.2012.01.039
State	Published - 23 Mar 2012
Externally published	Yes

Keywords

CDC
ERK1/2
HBXIP
NF-κB
mCRP

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.febslet.2012.01.039

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@article{29b530aaa2a4448c829e92470922269f,

title = "HBXIP upregulates CD46, CD55 and CD59 through ERK1/2/NF-κB signaling to protect breast cancer cells from complement attack",

abstract = "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. Crown",

keywords = "CDC, ERK1/2, HBXIP, NF-κB, mCRP",

author = "Wenjing Cui and Yu Zhao and Changliang Shan and Guangyao Kong and Nan Hu and Yiwen Zhang and Shuai Zhang and Weiying Zhang and Yingyi Zhang and Xiaodong Zhang and Lihong Ye",

year = "2012",

month = mar,

day = "23",

doi = "10.1016/j.febslet.2012.01.039",

language = "英语",

volume = "586",

pages = "766--771",

journal = "FEBS Letters",

issn = "0014-5793",

publisher = "John Wiley and Sons Inc",

number = "6",

}

TY - JOUR

T1 - HBXIP upregulates CD46, CD55 and CD59 through ERK1/2/NF-κB signaling to protect breast cancer cells from complement attack

AU - Cui, Wenjing

AU - Zhao, Yu

AU - Shan, Changliang

AU - Kong, Guangyao

AU - Hu, Nan

AU - Zhang, Yiwen

AU - Zhang, Shuai

AU - Zhang, Weiying

AU - Zhang, Yingyi

AU - Zhang, Xiaodong

AU - Ye, Lihong

PY - 2012/3/23

Y1 - 2012/3/23

N2 - 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. Crown

AB - 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. Crown

KW - CDC

KW - ERK1/2

KW - HBXIP

KW - NF-κB

KW - mCRP

UR - https://www.scopus.com/pages/publications/84862817326

U2 - 10.1016/j.febslet.2012.01.039

DO - 10.1016/j.febslet.2012.01.039

M3 - 文章

C2 - 22293503

AN - SCOPUS:84862817326

SN - 0014-5793

VL - 586

SP - 766

EP - 771

JO - FEBS Letters

JF - FEBS Letters

IS - 6

ER -

HBXIP upregulates CD46, CD55 and CD59 through ERK1/2/NF-κB signaling to protect breast cancer cells from complement attack

Abstract

Keywords

UN SDGs

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