MicroRNA‑126 exerts antitumor functions in ovarian cancer by targeting EGFL7 and affecting epithelial‑to‑mesenchymal transition and ERK/MAPK signaling pathway
- Yuhua Zhang
- Xiaobo Qin
- Juan Jiang
- Wenjie Zhao
Affiliations: Reproductive Medicine Centre, Weifang People's Hospital, Weifang, Shandong 261041, P.R. China, Department of Obstetrics and Gynecology, Zhangqiu District Maternal and Child Health Care Hospital, Jinan, Shandong 250200, P.R. China , Department of Nursing, The Third People's Hospital of Qingdao, Qingdao, Shandong 266041, P.R. China
- Published online on: May 29, 2020 https://doi.org/10.3892/ol.2020.11687
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Ovarian cancer (OC) is a common gynecological malignant carcinoma worldwide. Accumulating research has revealed that multiple microRNAs (miRNAs) are abnormally expressed at different levels in various malignancies, playing vital roles in tumorigenesis. This study investigated the regulatory functions and potential mechanism of miR‑126 in OC proliferation, invasion and migration. It was found that miR‑126 was prominently downregulated in OC. Moreover, the decrease of miR‑126 promoted the aggressive phenotypes and indicated poor prognosis of OC patients. Functional assays demonstrated that restoration of miR‑126 dramatically repressed OC cell proliferation, migration and invasion. Furthermore, luciferase reporter assay was conducted to verify putative binding sites of miR‑126 in the epidermal growth factor‑like domain 7 (EGFL7) 3' untranslated region (3'UTR), indicating that EGFL7 was a target gene of miR‑126 in OC cells. It was further discovered that miR‑126 exerts its function on regulating ERK/MAPK pathway and epithelial‑to‑mesenchymal transition (EMT) in OC cells. The above findings suggested that miR‑126 served as a cancer suppressor in OC, suggesting a promising application of miR‑126 in the clinical diagnosis and therapeutics of OC.