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Authors Wang Y, Shao F, Chen L
Received 8 July 2017
Accepted for publication 17 August 2017
Published 31 January 2018 Volume 2018:11 Pages 599—608
DOI https://doi.org/10.2147/OTT.S145864
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Akshita Wason
Peer reviewer comments 2
Editor who approved publication: Dr Samir Farghaly
Abstract: Epithelial ovarian cancer is the deadliest gynecological malignancy
worldwide. A better understanding of epithelial ovarian cancer pathogenesis and
the molecular mechanism underlying its metastasis may increase overall survival
rates. Previous studies have indicated that aldehyde dehydrogenase 1 family
member A2 (ALDH1A2) is a candidate tumor suppressor in epithelial ovarian
cancer. However, the potential role of ALDH1A2 in the molecular mechanisms of
epithelial ovarian cancer remains largely unclear. In the present study, we
found lower expression of ALDH1A2 in high-grade epithelial ovarian cancer
tissues than in low-grade epithelial ovarian cancer tissues. Overexpression of
ALDH1A2 decreased the proliferation and migration of epithelial ovarian cancer
cell lines, whereas ALDH1A2 knockdown significantly increased cell growth and
migration. Moreover, upregulation of ALDH1A2 also reduced the activation of
signal transducer and activator of transcription 3 (STAT3). In conclusion,
these findings suggest that ALDH1A2 suppresses epithelial ovarian cancer cell
proliferation and migration by downregulating STAT3.
Keywords: ALDH1A2,
epithelial ovarian cancer cell, STAT3, migration, cell growth