TY - JOUR
T1 - Stimulation of the estrogen axis induces epithelial-mesenchymal transition in human salivary cancer cells
AU - Sumida, Tomoki
AU - Ishikawa, Akiko
AU - Mori, Yoshihide
N1 - Funding Information:
This work was supported by JSPS KAKENHI Grant Number 15K11257. The Authors gratefully acknowledge this financial support. They would also like to thank Editage (www.editage.jp) for English language editing.
Publisher Copyright:
© 2016, International Institute of Anticancer Research. All rights reserved.
PY - 2016/7/1
Y1 - 2016/7/1
N2 - Background: Salivary gland cancer is a common type of head and neck cancer characterized by occasional deep invasion and lung metastasis. The precise role of sex steroid hormones in salivary gland cancer is unclear. To address this issue, we investigated whether the estrogen axis modulates salivary adenocarcinoma (SAC) and whether hormone therapy can be an effective treatment. Materials and Methods: The estrogen receptor (ER) was overexpressed in HSG human SAC cells that lack endogenous ER and the cells were treated with and without 17β-estradiol (E2). Results: E2 enhanced malignant phenotypes. Moreover, E2 treatment reduced E-cadherin expression, while increasing that of N-cadherin, vimentin, and inhibitor of differentiation 1 proteins that are associated with the epithelial-mesenchymal transition. Cell invasion was enhanced through activation of matrix metalloproteinase-9. Conclusion: These results indicate that hormone therapy used in breast cancer may also be effective for ER-positive SAC.
AB - Background: Salivary gland cancer is a common type of head and neck cancer characterized by occasional deep invasion and lung metastasis. The precise role of sex steroid hormones in salivary gland cancer is unclear. To address this issue, we investigated whether the estrogen axis modulates salivary adenocarcinoma (SAC) and whether hormone therapy can be an effective treatment. Materials and Methods: The estrogen receptor (ER) was overexpressed in HSG human SAC cells that lack endogenous ER and the cells were treated with and without 17β-estradiol (E2). Results: E2 enhanced malignant phenotypes. Moreover, E2 treatment reduced E-cadherin expression, while increasing that of N-cadherin, vimentin, and inhibitor of differentiation 1 proteins that are associated with the epithelial-mesenchymal transition. Cell invasion was enhanced through activation of matrix metalloproteinase-9. Conclusion: These results indicate that hormone therapy used in breast cancer may also be effective for ER-positive SAC.
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M3 - Article
C2 - 27365380
AN - SCOPUS:84977070540
SN - 1109-6535
VL - 13
SP - 305
EP - 310
JO - Cancer Genomics and Proteomics
JF - Cancer Genomics and Proteomics
IS - 4
ER -
