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Oncotarget. 2016 Oct 11;7(41):66558-66568. doi: 10.18632/oncotarget.11684.

Perfluorooctanoic acid induces human Ishikawa endometrial cancer cell migration and invasion through activation of ERK/mTOR signaling.

Author information

1
Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
2
Department of Obstetrics and Gynecology, Yangzhou Maternal and Child Health Hospital, Yangzhou University, Yangzhou, China.
3
State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China.
4
Key Laboratory of Pathogen Biology of Jiangsu Province, Nanjing Medical University, Nanjing, China.
5
Department of Microbiology, Nanjing Medical University, Nanjing, China.

Abstract

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.

KEYWORDS:

ERK/mTOR; PFOA; endometrial carcinoma; migration and invasion; tumorigenesis

PMID:
27589685
PMCID:
PMC5341820
DOI:
10.18632/oncotarget.11684
[Indexed for MEDLINE]
Free PMC Article

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