Literature DB >> 28485805

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

Y-P Liu1, X-H Sun, X-L Cao, W-W Jiang, X-X Wang, Y-F Zhang, J-L Wang.   

Abstract

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.

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Year:  2017        PMID: 28485805

Source DB:  PubMed          Journal:  Eur Rev Med Pharmacol Sci        ISSN: 1128-3602            Impact factor:   3.507


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