Abstract
The retroviral-vector-targeted CD59 gene (pSUPER-siCD59) was constructed and transfected into breast cells (MCF-7). The results demonstrated that the retroviral vector-mediated RNAi successfully suppressed human CD59 gene. The expression of CD59 decreased at both mRNA and protein levels. Knockdown of CD59 abrogated its protective effect on complement-mediated cytolysis. Fas and caspase-3 were remarkably upregulated, which induced apoptosis and tumor growth suppression in MCF-7 cells. In addition, overexpression of CD59 promoted the proliferation of MCF-7 cells and inhibited anti-apoptotic Bcl-2 expression. In conclusion, CD59 may be a promising target in the gene therapy of breast cancer.
Copyright © 2011 Elsevier Inc. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis / drug effects*
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Apoptosis / genetics
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Breast Neoplasms / genetics
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Breast Neoplasms / immunology
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Breast Neoplasms / pathology
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Breast Neoplasms / therapy*
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CD59 Antigens / genetics
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CD59 Antigens / immunology
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CD59 Antigens / metabolism*
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Caspase 3 / genetics
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Caspase 3 / metabolism
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Cell Line, Tumor
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Complement System Proteins / immunology
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Enzyme-Linked Immunosorbent Assay
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Female
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Gene Expression / drug effects*
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Gene Silencing / drug effects
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Humans
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Molecular Targeted Therapy / methods*
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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RNA, Messenger / analysis
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RNA, Messenger / biosynthesis
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RNA, Small Interfering / genetics
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RNA, Small Interfering / pharmacology*
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Retroviridae
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Reverse Transcriptase Polymerase Chain Reaction
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Transfection
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Up-Regulation / drug effects
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fas Receptor / genetics
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fas Receptor / metabolism
Substances
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CD59 Antigens
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FAS protein, human
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Proto-Oncogene Proteins c-bcl-2
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RNA, Messenger
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RNA, Small Interfering
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fas Receptor
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CD59 protein, human
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Complement System Proteins
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Caspase 3