Molecular Medicine Reports · 2018 · 15 citations · 33 references
MedicineCancer BiologyOncologyGene ExpressionMetastasisMolecular OncologyEsophageal CancerMalignant NeoplasmsMicrorna BiologyNoncoding Rna In CancerSquamous Cell CarcinomaTumor InvasionCancer Cell MigrationCell Migration AnalysisCell Proliferation IndicesMicrorna Function In CancerMicrorna In CancerMicrorna Regulation In CancerProtein Expression Levels
Esophageal cancer ranks fourth in cancer‑associated mortality in China and the incidence of esophageal adenocarcinoma has risen dramatically over the past two decades. MicroRNA (miRNA/miR) serves a pivotal role in human cancer cell growth, invasion and migration. MiR‑675‑3p is highly expressed in esophageal squamous cell cancer (ESCC) tissues, and may have an influence on ESCC cell migration and invasion. ESCC tumor tissue samples from 35 patients were profiled. MiR‑675‑3p expression was confirmed by reverse transcription‑quantitative polymerase chain reaction. Manipulation of miR‑675‑3p via knockdown was carried out with subsequent evaluation of effects on cell proliferation, invasion, migration, and use of western blotting and ELISA assays. MiR‑675‑3p was overexpressed in ESCC tissues compared with normal tissues, and had higher expression levels in ESCC cells compared with the healthy esophageal epithelial cell line. The results revealed a predominant upregulation of cell migration and invasion ability. MiR‑675‑3p inhibitor inhibited ESCC cell proliferation, migration and invasion ability. It was also demonstrated that downregulation of miR‑675‑3p decreased the levels of matrix metalloproteinase (MMP) 2 and 9 and increased the level of E‑cadherin. In addition, the effects of miR‑675‑3p inhibitor on ESCC cell lines were eliminated by con‑transfection with miR‑675‑3p inhibitor and miR‑675‑3p mimic. In conclusion, the results indicated that miR‑675‑3p may be involved in the progression of ESCC through regulating ESCC cell migration and invasion capacity via modulating epithelial mesenchymal transition markers (MMP2, MMP 9 and E‑cadherin).
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