Radiosensitizing effect of lapatinib in human epidermal growth factor receptor 2-positive breast cancer cells

Oncotarget. 2016 Nov 29;7(48):79089-79100. doi: 10.18632/oncotarget.12597.

Abstract

Trastuzumab has been widely used for the treatment of human epidermal growth factor receptor 2 (HER2)-overexpressing breast cancer, however, it cannot easily cross the blood-brain barrier (BBB) and is known to increase the incidence of brain metastases. In contrast, lapatinib has a low molecular weight and can cross the BBB and it could be useful to treat brain metastases in patients with HER2-positive breast cancer.To explore the impact of lapatinib on radiation response, we conducted an in vitro experiment using SKBR3 and BT474 breast carcinoma cells exhibiting HER2/neu amplification. Lapatinib down-regulated phosphorylated (p)-HER2, p-epidermal growth factor receptor, p-AKT, and p-extracellular signal-regulated kinase. Pretreatment of lapatinib increased the radiosensitivity of SKBR3 (sensitizer enhancement ratio [SER]: 1.21 at a surviving fraction of 0.5) and BT474 (SER: 1.26 at a surviving fraction of 0.5) cells and hindered the repair of DNA damage, as suggested by the prolongation of radiation-induced γH2AX foci and the down-regulation of phosphorylated DNA-dependent protein kinase, catalytic subunit (p-DNAPKcs). Increases in radiation-induced apoptosis and senescence were suggested to be the major modes of cell death induced by the combination of lapatinib and radiation. Furthermore, lapatinib did not radiosensitize a HER2- negative breast cancer cell line or normal human astrocytes.These findings suggest that lapatinib can potentiate radiation-induced cell death in HER2-overexpressing breast cancer cells and may increase the efficacy of radiotherapy. A phase II clinical trial using lapatinib concurrently with whole-brain radiation therapy (WBRT) is currently being conducted.

Keywords: breast cancer; human epidermal growth factor receptor 2; lapatinib; radiotherapy.

MeSH terms

  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / therapy
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Proliferation / radiation effects
  • Cell Survival / drug effects
  • Cell Survival / radiation effects
  • DNA-Activated Protein Kinase / metabolism
  • Female
  • Gene Amplification
  • Gene Expression Regulation, Neoplastic / drug effects
  • Gene Expression Regulation, Neoplastic / radiation effects
  • Humans
  • Lapatinib
  • MCF-7 Cells
  • Nuclear Proteins / metabolism
  • Phosphorylation
  • Quinazolines / pharmacology*
  • Radiation-Sensitizing Agents / pharmacology*
  • Receptor, ErbB-2 / genetics
  • Receptor, ErbB-2 / metabolism*

Substances

  • Nuclear Proteins
  • Quinazolines
  • Radiation-Sensitizing Agents
  • Lapatinib
  • ERBB2 protein, human
  • Receptor, ErbB-2
  • DNA-Activated Protein Kinase
  • PRKDC protein, human