Abstract
Because breast cancer patient survival inversely correlates with metastasis, we engineered vehicles to inhibit both the C-X-C chemokine receptor type 4 (CXCR4) and lipocalin-2 (Lcn2) mediated migratory pathways. pH-responsive liposomes were designed to protect and trigger the release of Lcn2 siRNA. Liposomes were modified with anti-CXCR4 antibodies to target metastatic breast cancer (MBC) cells and block migration along the CXCR4-CXCL12 axis. This synergistic approach--coupling the CXCR4 axis blockade with Lcn2 silencing--significantly reduced migration in triple-negative human breast cancer cells (88% for MDA-MB-436 and 92% for MDA-MB-231). The results suggested that drug delivery vehicles engineered to attack multiple migratory pathways may effectively slow progression of MBC.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Acute-Phase Proteins / antagonists & inhibitors*
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Acute-Phase Proteins / genetics
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Acute-Phase Proteins / metabolism
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Antibodies, Monoclonal / pharmacology*
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Apoptosis
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Blotting, Western
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Cell Movement*
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Cell Proliferation
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Combined Modality Therapy
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Drug Delivery Systems
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Drug Synergism
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Female
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Fluorescent Antibody Technique
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Gene Expression Regulation, Neoplastic*
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Humans
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Hydrogen-Ion Concentration
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Lipocalin-2
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Lipocalins / antagonists & inhibitors*
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Lipocalins / genetics
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Lipocalins / metabolism
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Liposomes
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Proto-Oncogene Proteins / antagonists & inhibitors*
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / metabolism
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RNA, Small Interfering / administration & dosage
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RNA, Small Interfering / genetics*
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Receptors, CXCR4 / antagonists & inhibitors*
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Receptors, CXCR4 / immunology
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Receptors, CXCR4 / metabolism
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Signal Transduction
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Triple Negative Breast Neoplasms / secondary
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Triple Negative Breast Neoplasms / therapy*
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Tumor Cells, Cultured
Substances
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Acute-Phase Proteins
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Antibodies, Monoclonal
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LCN2 protein, human
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Lipocalin-2
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Lipocalins
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Liposomes
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Proto-Oncogene Proteins
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RNA, Small Interfering
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Receptors, CXCR4