EGF receptor and p185erbB-2-specific single-chain antibody toxins differ in their cell-killing activity on tumor cells expressing both receptor proteins

Int J Cancer. 1995 Jan 3;60(1):137-44. doi: 10.1002/ijc.2910600120.

Abstract

Many human tumors over-express erbB-2 and EGF receptors. The membrane localization of these receptor tyrosine kinases make them appropriate targets for directed tumor therapy. We have used recombinant DNA technology to produce single-chain antibody exotoxin A (scFv-ETA) fusion proteins which specifically bind the erbB-2 and EGF receptors. The scFv portion is composed of the heavy- and light-chain variable domains of monoclonal antibodies which recognize the extracellular portion of each receptor. We have previously described the anti-tumor activity of the bacterially produced scFv(FRP5)-ETA directed to the erbB-2 receptor. In this paper we describe the characteristics of scFv(225)-ETA, a protein which binds the EGF receptor. The bacterially produced recombinant protein binds to the receptor with high affinity and inhibits the in vitro growth of the EGF receptor over-expressing tumor cell lines A431 and MDA-MB468. Combination treatment with scFv-(FRP5)-ETA and scFv(225)-ETA led to an additive inhibitory effect on the in vitro growth of A431 cells. SKBR3 cells expressing low levels of EGF receptor but high levels of p185erbB-2 were not affected by scFv(225)-ETA treatment but were sensitive to scFv(FRP5)-ETA. Stimulation of SKBR3 cells and HCII RI#11 mouse mammary epithelial cells expressing the human erbB-2 with EGF led to an increase in scFv(FRP5)-ETA activity, showing that the EGF-induced activation of erbB-2 can potentiate the action of the erbB-2-directed toxin. Treatment of athymic nude mice with scFv(FRP5)-ETA and the combination of both scFv-ETA proteins led to the transient arrest of growth of established A431 tumors. scFv(225)-ETA treatment alone was the most effective, leading to tumor shrinkage during the course of treatment, whereas treatment with the parental monoclonal antibody 225 led to retarded tumor growth.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • ADP Ribose Transferases*
  • Amino Acid Sequence
  • Animals
  • Antibodies, Monoclonal
  • Antibody Specificity
  • Bacterial Toxins*
  • Base Sequence
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / ultrastructure*
  • Carcinoma, Squamous Cell / drug therapy*
  • Carcinoma, Squamous Cell / ultrastructure*
  • Cell Division / drug effects
  • Cell Survival / drug effects
  • ErbB Receptors / genetics
  • ErbB Receptors / immunology*
  • ErbB Receptors / metabolism
  • Exotoxins / genetics
  • Exotoxins / toxicity*
  • Female
  • Humans
  • Immunotoxins / toxicity*
  • Mice
  • Mice, Nude
  • Molecular Sequence Data
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / immunology*
  • Neoplasm Proteins / metabolism
  • Pseudomonas aeruginosa Exotoxin A
  • Receptor, ErbB-2 / genetics
  • Receptor, ErbB-2 / immunology*
  • Receptor, ErbB-2 / metabolism
  • Recombinant Fusion Proteins / genetics
  • Recombinant Fusion Proteins / toxicity
  • Sensitivity and Specificity
  • Virulence Factors*
  • Vulvar Neoplasms / drug therapy*
  • Vulvar Neoplasms / ultrastructure*

Substances

  • Antibodies, Monoclonal
  • Bacterial Toxins
  • Exotoxins
  • Immunotoxins
  • Neoplasm Proteins
  • Recombinant Fusion Proteins
  • Virulence Factors
  • ADP Ribose Transferases
  • ErbB Receptors
  • Receptor, ErbB-2