MiR-96-5p promotes the proliferation, invasion and metastasis of papillary thyroid carcinoma through down-regulating CCDC67

Z.-M. Liu, Z.-Y. Wu, W.-H. Li, L.-Q. Wang, J.-N. Wan, Y. Zhong

Department of Thyroid and Breast Surgery, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. mark-wang@163.com

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• Oncology

OBJECTIVE: MicroRNAs (miRNAs) have been identified to play an important regulatory role in various biological behaviors of papillary thyroid carcinoma (PTC). However, the specific role and function of miR-96-5p in PTC remain unclear. Therefore, the aim of this study is to detect the expression of miR-96-5p in PTC, and to explore its exact function.
PATIENTS AND METHODS: The relative expression level of miR-96-5p in PTC tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). MiR-96-5p mimics or inhibitors were then constructed and transfected into cells to upregulate or downregulate miR-96-5p expression. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay and colony formation assay were employed to evaluate the proliferation of PTC cells. Meanwhile, transwell assay was employed to detect the invasion and metastasis of PTC cells. In addition, the underlying mechanism of miR-96-5p was identified by Luciferase reporter gene assay and Western blot analysis.
RESULTS: The expression of miR-96-5p in PTC tissues and PTC-derived cell lines was significantly higher than that of normal controls. The overexpression of miR-96-5p remarkably promoted the proliferation, invasion and migration of PTC cells. However, knockdown of miR-96-5p significantly decreased cell growth and metastasis. CCDC67 was verified as a target gene of miR-96-5p in PTC. Further experiments demonstrated that the restoration of CCDC67 could significantly reduce the carcinogenic function of miR-96-5p.
CONCLUSIONS: MiR-96-5p was remarkably upregulated in PTC tumor tissues and cells. In addition, it promoted cell growth, invasion, and migration via repressing CCDC67 expression.

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