Abstract
Recently, many mircroRNAs (miRNAs) involved in the development and progression of cancer have been reported to regulate cell growth and metastasis, including microRNA-202 (miR-202). The purpose of the present study was to elucidate the effect of miR-202 on endometrial carcinoma (EC) cell migration and invasion. First, qRT-PCR showed that miR-202 was down-regulated in EC tissues, which was associated with poor prognosis in EC patients. Functionally, transwell assay indicated that miR-202 inhibited cell migration and invasion in EC cells. In addition, miR-202 also blocked epithelial–mesenchymal transition (EMT) through suppressing N-cadherin and Vimentin expressions and promoting E-cadherin expression. Moreover, the dual-luciferase reporter assay showed that fibroblast growth factor 2 (FGF2) is a direct target gene for miR-202 in EC cells. Furthermore, up-regulation of FGF2 attenuated the inhibitory effect of miR-202 on cell migration and invasion in EC. Besides that, miR-202 inactivated the Wnt/β-catenin signaling by suppressing β-catenin expression in EC. In conclusion, miR-202 inhibited cell migration and invasion by targeting FGF2 and inactivating the Wnt/β-catenin signaling in EC.
Highlights
Endometrial cancer (EC) has become a major threat to women’s health and its incidence is increasing [1]
The results showed that the expression of miR-202 in EC tissues was lower than in normal tissues (Figure 1A)
Low miR-202 expression was associated with shorter overall survival in EC patients, suggesting that low miR-202 expression predicts poor prognosis in EC patients (Figure 1B)
Summary
Endometrial cancer (EC) has become a major threat to women’s health and its incidence is increasing [1]. Some EC patients have a risk of cancer recurrence and death, and those patients that relapse have a poor prognosis [4]. There has been extensive investigation into the roles of mircroRNAs (miRNAs) in EMT and cell metastasis. One study found that miR-101-3p attenuated the metastasis of glioblastoma cells by inhibiting EMT [6]. MiR-103 was found to promote metastasis and EMT by directly inhibiting the expression of LATS2 in hepatocellular carcinoma [7]. MiR-23a was shown to inhibit EMT in EC via targeting SMAD3 [8], while miR-652 was reported to promote proliferation and metastasis of EC cells by regulating RORA expression [9]. MiR-202 may play an important role in different cancers. MiR-202 suppressed cell proliferation in EC by targeting FOXR2 [10], and low miR-202 expression was shown to contribute
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