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Colony-stimulating factor-1 antibody reverses chemoresistance in human MCF-7 breast cancer xenografts

Cancer Res. 2006 Apr 15;66(8):4349-56. doi: 10.1158/0008-5472.CAN-05-3523.

Abstract

Overexpression of colony-stimulating factor-1 (CSF-1) and its receptor in breast cancer is correlated with poor prognosis. Based on the hypothesis that blockade of CSF-1 would be beneficial in breast cancer treatment, we developed a murinized, polyethylene glycol-linked antigen-binding fragment (Fab) against mouse (host) CSF-1 (anti-CSF-1 Fab). Mice bearing human, chemoresistant MCF-7 breast cancer xenografts were treated with combination chemotherapy (CMF: cyclophosphamide, methotrexate, 5-fluorouracil; cycled twice i.p.), anti-CSF-1 Fab (i.p., cycled every 3 days for 14 days), combined CMF and anti-CSF-1 Fab, or with Ringer's solution as a control. Anti-CSF-1 Fab alone suppressed tissue CSF-1 and retarded tumor growth by 40%. Importantly, in combination with CMF, anti-CSF-1 Fab reversed chemoresistance of MCF-7 xenografts, suppressing tumor development by 56%, down-regulating expression of the chemoresistance genes breast cancer-related protein, multidrug resistance gene 1, and glucosylceramide synthase, and prolonging survival significantly. Combined treatment also reduced angiogenesis and macrophage recruitment and down-regulated tumor matrix metalloproteinase-2 (MMP-2) and MMP-12 expression. These studies support the paradigm of CSF-1 blockade in the treatment of solid tumors and show that anti-CSF-1 antibodies are potential therapeutic agents for the treatment of mammary cancer.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Combined Chemotherapy Protocols / administration & dosage
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology*
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / enzymology
  • Breast Neoplasms / immunology
  • Breast Neoplasms / pathology
  • Cell Growth Processes / drug effects
  • Cell Growth Processes / physiology
  • Cell Line, Tumor
  • Cyclophosphamide / administration & dosage
  • DNA Primers
  • Down-Regulation / drug effects
  • Drug Resistance, Multiple
  • Drug Resistance, Neoplasm
  • Fluorouracil / administration & dosage
  • Humans
  • Immunoglobulin Fragments / chemistry
  • Immunoglobulin Fragments / immunology
  • Immunoglobulin Fragments / pharmacology*
  • Macrophage Colony-Stimulating Factor / antagonists & inhibitors*
  • Macrophage Colony-Stimulating Factor / biosynthesis
  • Macrophage Colony-Stimulating Factor / genetics
  • Macrophage Colony-Stimulating Factor / immunology
  • Matrix Metalloproteinases / biosynthesis
  • Matrix Metalloproteinases / genetics
  • Methotrexate / administration & dosage
  • Mice
  • RNA, Messenger / genetics
  • Receptor, Macrophage Colony-Stimulating Factor / genetics
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor Receptor-1 / genetics
  • Vascular Endothelial Growth Factor Receptor-2 / genetics
  • Xenograft Model Antitumor Assays

Substances

  • DNA Primers
  • Immunoglobulin Fragments
  • RNA, Messenger
  • Vascular Endothelial Growth Factor A
  • Macrophage Colony-Stimulating Factor
  • Cyclophosphamide
  • FLT1 protein, human
  • Receptor, Macrophage Colony-Stimulating Factor
  • Vascular Endothelial Growth Factor Receptor-1
  • Vascular Endothelial Growth Factor Receptor-2
  • Matrix Metalloproteinases
  • Fluorouracil
  • Methotrexate

Supplementary concepts

  • CMF regimen