Journal
ONCOTARGET
Volume 7, Issue 41, Pages 66558-66568Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.11684
Keywords
endometrial carcinoma; PFOA; migration and invasion; tumorigenesis; ERK/mTOR
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Funding
- National Natural Science Foundation of China [81372850]
- Key University Natural Science Research Project of Jiangsu Province [15KJA320003]
- Jiangsu Entrepreneurship & Innovation Award
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Perfluorooctanoic acid (PFOA) is a common environmental pollutant that has been associated with various diseases, including cancer. We explored the molecular mechanisms underlying PFOA-induced endometrial cancer cell invasion and migration. PFOA treatment enhanced migration and invasion by human Ishikawa endometrial cancer cells, which correlated with decreased E-cadherin expression, a marker of epithelial-mesenchymal transition. PFOA also induced activation of ERK1/2/mTOR signaling. Treatment with rapamycin, an mTOR inhibitor, antagonized the effects of PFOA and reversed the effects of PFOA activation in a xenograft mouse model of endometrial cancer. Consistent with these results, pre-treatment with rapamycin abolished PFOA-induced down-regulation of E-cadherin expression. These results indicate that PFOA is a carcinogen that promotes endometrial cancer cell migration and invasion through activation of ERK/mTOR signaling.
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