Journal
ONCOLOGY REPORTS
Volume 31, Issue 5, Pages 2021-2028Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2014.3106
Keywords
ovarian carcinoma; epithelial-to-mesenchymal transition; miR-101; ZEB1; ZEB2
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Funding
- Blanton-Davis Ovarian Cancer Research Program
- University of Texas M.D. Anderson Cancer Center, National Institutes of Health [CA016672]
- China Education Council
- Diane Denson Tobola Fellowship in Ovarian Cancer Research
- Harold C. and Mary L. Daily Endowment Fund
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Ovarian carcinoma is the most lethal gynecologic malignancy; the majority of patients succumb to the disease within 5 years of diagnosis. The poor survival rate is attributed to diagnosis at advanced stage, when the tumor has metastasized. The epithelial-to-mesenchymal transition (EMT) is a necessary step toward metastatic tumor progression. Through integrated computational analysis, we recently identified a master microRNA (miRNA) network that includes miR-101 and regulates EMT in ovarian carcinoma. In the present study, we characterized the functions of miR-101. Using reporter gene assays, we demonstrated that miR-101 suppressed the expression of the E-cadherin repressors ZEB1 and ZEB2 by directly targeting the 3'-untranslated region (3'UTR) of both ZEB1 and ZEB2. Introduction of miR-101 significantly inhibited EMT and cell migration and invasion. Introducing cDNAs of ZEB1 and ZEB2 without 3'UTR abrogated miR-101-induced EMT alteration, respectively. Our findings showed that miR-101 represents a redundant mechanism for the miR-200 family that regulates EMT through two major E-cadherin transcriptional repressors.
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