DNA strand breaks and cell cycle perturbation in herceptin treated breast cancer cell lines

Breast Cancer Res Treat. 2001 Nov;70(2):123-9. doi: 10.1023/a:1012999012192.

Abstract

Background: Herceptin is a humanized antibody that binds to the product of the HER-2 oncogene. Clinical studies have indicated that treatment with Herceptin may slow disease progression in tumors expressing high levels of the HER-2 antigen. However, the mechanism of this action is not known.

Methods: Four different cell lines were used that had different levels of HER-2 expression. Treated and nontreated cells were analyzed for DNA strand breaks and cell cycle perturbation using standard flow cytometry methods.

Results: In this study we found that cell lines expressing high levels of HER-2, when treated with Herceptin, exhibited marked increases in DNA strand breaks as measured by the TUNEL assay, and that these cells also exhibited slowed growth. BT-474 and SKBR-3 cell lines, both of which express high levels of the HER-2 antigen, had significant increases in labeled nucleotide expression at 3 and 6 day time points following exposure to Herceptin at a concentration of 10 microg/ml. Similar treatment of MCF-7 and MDA-231 cell lines, both of which express low levels of HER-2, had little effect on the level of labeled nucleotide expression at either the 3 or 6 day time points. Following 4 days of Herceptin treatment, BT-474 and SKBR-3 cell lines had significant decreases in the percentage of cells in the S phase of growth. This effect was not seen in either the MCF-7 or MDA-231 cell lines.

Conclusion: Herceptin has a biological effect only on cells that contain high levels of HER-2. This effect is a decrease in cell proliferation that is coincident with, and may be caused by an increase frequency of DNA strand breaks.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Antibodies, Monoclonal / pharmacology*
  • Antibodies, Monoclonal / therapeutic use
  • Antibodies, Monoclonal, Humanized
  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents / therapeutic use
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / genetics
  • Breast Neoplasms / pathology
  • Cell Cycle / drug effects*
  • Cell Division / drug effects
  • DNA Damage*
  • Humans
  • Receptor, ErbB-2 / analysis
  • Receptor, ErbB-2 / biosynthesis
  • Trastuzumab
  • Tumor Cells, Cultured / drug effects

Substances

  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Humanized
  • Antineoplastic Agents
  • Receptor, ErbB-2
  • Trastuzumab