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.
Copyright © 2012. Published by Elsevier B.V.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adaptor Proteins, Signal Transducing / immunology*
-
Animals
-
Breast Neoplasms / immunology*
-
CD55 Antigens / immunology*
-
CD59 Antigens / immunology*
-
Complement Activation / immunology
-
Complement System Proteins / immunology*
-
Female
-
Humans
-
MAP Kinase Signaling System / immunology*
-
Membrane Cofactor Protein / immunology*
-
Mice
-
Mice, Nude
-
Mitogen-Activated Protein Kinase 1 / metabolism
-
Mitogen-Activated Protein Kinase 3 / metabolism
-
NF-kappa B / immunology*
-
Trans-Activators / immunology
-
Tumor Cells, Cultured
-
Viral Regulatory and Accessory Proteins
Substances
-
Adaptor Proteins, Signal Transducing
-
CD55 Antigens
-
CD59 Antigens
-
LAMTOR5 protein, human
-
Membrane Cofactor Protein
-
NF-kappa B
-
Trans-Activators
-
Viral Regulatory and Accessory Proteins
-
hepatitis B virus X protein
-
Complement System Proteins
-
MAPK1 protein, human
-
Mitogen-Activated Protein Kinase 1
-
Mitogen-Activated Protein Kinase 3