MicroRNA-217 suppressed epithelial-to-mesenchymal transition in gastric cancer metastasis through targeting PTPN14.

OBJECTIVE: Gastric cancer (GC) is the third leading cause of cancer-related deaths while the mechanisms underlying its metastasis are not fully understood. In this study, we aimed to explore the relationship between miR-217 and GC metastasis.

PATIENTS AND METHODS: We examined miR-217 level in gastric tumor tissues of 48 patients with GC and in cell lines including gastric mucosa epithelial cell line (GES-1), gastric cancer cell line (BGC-823), and gastric cancer cell line (SGC-7901). The effects of miR-217 on EMT conditions were detected using cell migration and invasion assays. The potential regulatory target of miR-217 was determined by prediction tool, target protein expression and Luciferase reporter assay.

RESULTS: We found a lower expression of miR-217 in the tumor tissues of GC patients with metastasis. Increased expression of miR-217 markedly suppressed GC cell metastasis and invasion in vitro. We observed a strongly negative correlation between expressions of miR-217 and PTPN14 mRNA in GC tissues, and miR-217 repressed PTPN14 expression by directly targeting its 3'UTR. Furthermore, the loss of PTPN14 induced by miR-217 or si-PTPN14 reduced the metastasis and invasion of GC cells, whereas restoration of PTPN14 led to the enhanced metastases and invasion of GC cells. MiR-217-induced the loss of PTPN14 modulated the epithelial-to-mesenchymal transition (EMT) in GC cells, as indicated by the modulated expression of E-cadherin.

CONCLUSIONS: We concluded that miR-217 suppressed the EMT through directly binding to the PTPN14-3'UTR in GC progression, and might be a novel biomarker for the detection of GC metastasis.