miR-373-3p inhibits EMT via regulation of TGFβR2 in choriocarcinoma
Abstract Background: Previous studies have indicated that early metastasis is a major cause of mortality in patients with choriocarcinoma. However, what determines whether early metastasis of choriocarcinoma has occurred is unknown. The emerging role of miRNA in regulating cancer development and progression has been recognized. MiR-373-3p has been shown to play pivotal roles in tumorigenesis and metastasis. However, whether miR-373-3p functions to promote choriocarcinoma metastasis is not clear. The purpose of this study is to determine the function of miR-373-3p in the progression of choriocarcinoma. Methods: In this study, we first compared EMT-related markers, which are inversely correlated with miR-373-3p expression, in trophoblast and choriocarcinoma cell lines. Using PCR and western blot, the upregulation of miR‑373‑3p was observed to inhibit EMT progression. Similarly, gain-and loss-of-function studies revealed that ectopic miR-373-3p overexpression inhibited the metastasis of choriocarcinoma cells. Results: Our results revealed that miR-373-3p functions as an inhibitor in JEG-3 and JAR cells; this is due to its mediation of the TGF-β signalling pathway, which is responsible for EMT. The bioinformatic analysis and dual‑luciferase reporter gene assays were employed to verify that miR‑373‑3p might interact with the 3' untranslated region of TGFβR2 mRNA. Further western blot results showed miR‑373‑3 preversed the increases of TGFβR2 and inhibited EMT. Conclusions: In light of our observations, miR‑373‑3p upregulation partly accounts for TGFβR2 downregulation and leads to a restraint of EMT and metastasis. MiR‑373‑3p may, therefore, serve as a valuable target in potential anticancer strategies to treat choriocarcinoma.