MicroRNA?203 inhibits papillary thyroid cancer metastasis via directly targeting Bmi-1
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Background:The oncogene B-cell-specific Moloney murine leukemia virus insertion site?1 (Bmi-1) is overexpressed in papillary thyroid cancer(PTC). Previous study demonstrated that Bmi-1is highly expressed in several types of cancer.Translational regulation has emerged as a prominent underlying mechanism of Bmi-1 regulation, particularly via microRNA targeting.
Methods:Quantitative RT-PCR was used to measure Bmi-1 and miR-203 expression in PTC tissues and cell lines. The cell Transwell invasion assays were performed. A luciferase reporter assay was conducted to confirm the target gene of miR-203, and the results were validated in PTC cell lines and tissues.
Results: Bmi-1 was outstandingly increased in PTC tissues compared with normal thyroid and nodular goiter respectively. What’s more, Bmi-1 may be directly targeted by miR?203 using a luciferase assay in PTC. In addition, enforced expression of miR-203 led to significant downregulation of Bmi-1 protein and mRNA expression levels. Furthermore, transfection of miR-203 significantly inhibited cell migration in PTC cells. miR?203 was downregulated in PTC patients, and a negative correlation between the expression of miR?203 and Bmi-1 was observed. The results of the present study indicated that miR?203 exerts cell migration effects in PTC through the suppression of Bmi-1 expression.
Conclusions:In conclusion, the present study demonstrated that Bmi-1 is up-regulated in PTC and enhanced migration ability of PTC cells by being regulated by miR-203.
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