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Assessment of Ethanol Induction of Breast Cancer Metastasis: the Involvement of ErbB2 and Endoplasmic Reticulum (ER) Stress (LB833)
Author(s) -
Pan Daniel,
Xu Mei,
Luo Jia
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb833
Subject(s) - breast cancer , endoplasmic reticulum , metastasis , cancer , cancer research , ethanol , phosphorylation , medicine , unfolded protein response , cancer cell , chemistry , endocrinology , biology , microbiology and biotechnology , biochemistry
Ethanol consumption is a risk factor for the development of breast cancer and a possible promoter of breast cancer metastasis. However, the mechanisms of oncogenic action are still unknown. Previous studies have shown that breast cancer cells over‐expressing ErbB2 have been more susceptible to ethanol‐induced invasion and migration and that ER stress also promotes tumor metastasis. The objective of this study is to determine whether ethanol exposure may activate ErbB2 and induce ER stress in breast cancer cells. In this study, we test this hypothesis by examining the effect of ethanol on the activation of ErbB2 and eIF2α/PKR. The enhanced phosphorylation of eIF2α and PKR are considered indicators of ER stress. MCF7 human breast cancer cells were treated with or without ethanol for 20 days. The results indicated that phosphorylated ErbB2 was increased by a factor of 1.4 in cells treated with 0.1% ethanol and by a factor of 1.2 for cells treated with 0.2% ethanol when compared to the untreated control. Also, phosphorylated eIF2α was shown to have a 1.3 and 1.2 fold increase in 0.1% and 0.2% ethanol, respectively, while phospho‐PKR was shown to have a 1.7 and 1.5 fold increase for 0.1% and 0.2% ethanol, respectively. These findings suggest that ethanol can activate ErbB2 and induce ER stress in breast cancer cells, which may result in increased metastasis. This study was supported by NIH grant (AA017226). Grant Funding Source : Supported by NIH grant (AA017226)