原创力文档arsenic, cadmium and neuron specific enolase (eno2, γ-enolase) expression in breast cancer砷、镉和神经元特异性烯醇酶(eno2γ-enolase)表达在乳腺癌.pdfVIP
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arsenic, cadmium and neuron specific enolase (eno2, γ-enolase) expression in breast cancer砷、镉和神经元特异性烯醇酶(eno2γ-enolase)表达在乳腺癌
Soh et al. Cancer Cell International 2011, 11:41
/content/11/1/41
PRIMARY RESEARCH Open Access
Arsenic, cadmium and neuron specific enolase
(ENO2, g-enolase) expression in breast cancer
1 1 1 2 1 1
Maureen A Soh , Scott H Garrett , Seema Somji , Jane R Dunlevy , Xu Dong Zhou , Mary Ann Sens ,
Chandra S Bathula1, Christina Allen1 and Donald A Sens1*
Abstract
Background: Neuron specific enolase (ENO2, g-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+3 and Cd+2 sufficient 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+3 and Cd+2 exposure 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+3 or Cd+2. Localization studies showed that ENO2 in
the MCF-10A cells transformed by As+3 or Cd+2 had 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+3 or Cd+2. The findings also suggest a possible link between As+3 and Cd+2 exposure
and neuroendocrine differentiation in tumors. Overall, the results suggest t
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