Arsenic, cadmium and neuron specific enolase (ENO2, γ-enolase) expression in breast cancer

Abstract

Background: Neuron specific enolase (ENO2, γ-enolase) has been used as a biomarker to help identify neuroendocrine differentiation in breast cancer. The goal of the present study was to determine if ENO2 expression in the breast epithelial cell is influenced by the environmental pollutants, arsenite and cadmium. Acute and chronic exposure of MCF-10A cells to As+3and Cd+2sufficient to allow colony formation in soft agar, was used to determine if ENO2 expression was altered by these pollutants.Results: It was shown that both As+3and Cd+2exposure caused significant increases in ENO2 expression under conditions of both acute and chronic exposure. In contrast, ENO1, the major glycolytic enolase in non-muscle and neuronal cells, was largely unaffected by exposure to either As+3or Cd+2. Localization studies showed that ENO2 in the MCF-10A cells transformed by As+3or Cd+2had both a cytoplasmic and nuclear localization. In contrast, ENO1 was localized to the cytoplasm. ENO2 localized to the cytoplasm was found to co-localized with ENO1.Conclusion: The results are the first to show that ENO2 expression in breast epithelial cells is induced by acute and chronic exposure to As+3or Cd+2. The findings also suggest a possible link between As+3and Cd+2exposure and neuroendocrine differentiation in tumors. Overall, the results suggest that ENO2 might be developed as a biomarker indicating acute and/or chronic environmental exposure of the breast epithelial cell to As+3and Cd+2. © 2011 Soh et al; licensee BioMed Central Ltd.