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MicroRNA-298 inhibits malignant phenotypes of epithelial ovarian cancer by regulating the expression of EZH2

  • Authors:
    • Fenmei Zhou
    • Juan Chen
    • Hairong Wang
  • View Affiliations / Copyright

    Affiliations: Department of Obstetrics and Gynecology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China, Huai'an Maternal and Child Healthcare Center, Huai'an, Jiangsu 223302, P.R. China
    Copyright: © Zhou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 3926-3932
    |
    Published online on: September 29, 2016
       https://doi.org/10.3892/ol.2016.5204
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Abstract

MicroRNA (miRNA or miR)-298 has been reported to be downregulated and to modify the expression of the polycomb protein enhancer of zeste 2 (EZH2) in recurrent epithelial ovarian cancer (EOC). To date, no functional evidence of a miR-298-EZH2 axis in EOC has been documented. The present study aimed to investigate the associations of miR‑298 and/or EZH2 expression with clinicopathological features of EOC patients, and revealed their roles in cell motility based on EOC cell lines. Reverse transcription-quantitative polymerase chain reaction was performed to detect the expression levels of miR‑298 and EZH2 messenger RNA in human EOC tissues and cell lines. Wound healing and transwell assays were performed to determine the function of the miR‑298‑EZH2 axis on cell migration and invasion, respectively. Compared with normal tissues, miR‑298 expression was significantly downregulated, while EZH2 expression was significantly upregulated, in human EOC tissues (both P=0.001). In addition, miR‑298 downregulation and EZH2 upregulation were significantly associated with high clinical stage (both P=0.01) and pathological grade (both P=0.02) of EOC patients. Furthermore, the ectopic expression of miR‑298 could efficiently inhibit cell migration and invasion. Notably, the overexpression of EZH2 could restore the cell migration and invasion abilities suppressed by miR‑298. Our data offer convincing evidence that the dysregulation of the miR‑298‑EZH2 axis may be important in tumor progression of EOC patients. The present study also confirmed a tumor‑suppressive role of miR‑298 in modulating EOC cell motility by regulating the expression of EZH2, implying its potential as a novel miRNA‑based therapeutic target for the treatment of human EOC.
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Copy and paste a formatted citation
Spandidos Publications style
Zhou F, Chen J and Wang H: MicroRNA-298 inhibits malignant phenotypes of epithelial ovarian cancer by regulating the expression of EZH2. Oncol Lett 12: 3926-3932, 2016.
APA
Zhou, F., Chen, J., & Wang, H. (2016). MicroRNA-298 inhibits malignant phenotypes of epithelial ovarian cancer by regulating the expression of EZH2. Oncology Letters, 12, 3926-3932. https://doi.org/10.3892/ol.2016.5204
MLA
Zhou, F., Chen, J., Wang, H."MicroRNA-298 inhibits malignant phenotypes of epithelial ovarian cancer by regulating the expression of EZH2". Oncology Letters 12.5 (2016): 3926-3932.
Chicago
Zhou, F., Chen, J., Wang, H."MicroRNA-298 inhibits malignant phenotypes of epithelial ovarian cancer by regulating the expression of EZH2". Oncology Letters 12, no. 5 (2016): 3926-3932. https://doi.org/10.3892/ol.2016.5204
Copy and paste a formatted citation
x
Spandidos Publications style
Zhou F, Chen J and Wang H: MicroRNA-298 inhibits malignant phenotypes of epithelial ovarian cancer by regulating the expression of EZH2. Oncol Lett 12: 3926-3932, 2016.
APA
Zhou, F., Chen, J., & Wang, H. (2016). MicroRNA-298 inhibits malignant phenotypes of epithelial ovarian cancer by regulating the expression of EZH2. Oncology Letters, 12, 3926-3932. https://doi.org/10.3892/ol.2016.5204
MLA
Zhou, F., Chen, J., Wang, H."MicroRNA-298 inhibits malignant phenotypes of epithelial ovarian cancer by regulating the expression of EZH2". Oncology Letters 12.5 (2016): 3926-3932.
Chicago
Zhou, F., Chen, J., Wang, H."MicroRNA-298 inhibits malignant phenotypes of epithelial ovarian cancer by regulating the expression of EZH2". Oncology Letters 12, no. 5 (2016): 3926-3932. https://doi.org/10.3892/ol.2016.5204
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