MircoRNA-629 promotes proliferation, invasion and migration of nasopharyngeal carcinoma through targeting PDCD4

Y.-Q. Zheng, Y.-F. Bai, S. Yang, Y.-R. Cui, Y.-P. Wang, W.-L. Hu

Department of Otorhinolaryngology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China. huwenliang6688@163.com

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• Oncology

OBJECTIVE: MicroRNAs (miRNA) have been demonstrated to be involved in the development and progression of several tumors, including nasopharyngeal carcinoma (NPC). However, the expression and function of miR-629 in NPC have not been elucidated before. Here, we explored the role of miR-629 in NPC cells and investigated the possible underlying mechanism.

MATERIALS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was first utilized to detect the expression of miR-629 in NPC tissues and adjacent normal samples, as well as NPC cell lines and normal nasopharyngeal cell line NP69. MiR-629 mimics and inhibitor was transfected in NPC cells to up-regulate or down-regulate the expression of miR-629. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay and flow cytometry were used to explore the effects of miR-629 on the proliferation and cell circle of established NPC cells, respectively. Cell invasion and migration abilities were evaluated by transwell Matrigel assay and wound healing assay. Meanwhile, the underlying mechanism of miR-629 in NPC was detected using bioinformatics prediction and dual-luciferase analysis. In addition, Western blotting was employed to identify the expression of the miR-629 targeted protein.

RESULTS: MiR-629 expression in NPC tissues was significantly higher than that of adjacent normal samples. Expression of miR-629 in NPC cells was significantly higher than that NP69 cells. Over-expressing miR-629 remarkably promoted 6-10B cell proliferation, while knocking down miR-629 significantly inhibited 5-8F cell growth compared with negative control group. Cell migration and invasion abilities were remarkably increased by miR-629 mimics transfection. However, the miR-629 inhibitor transfection in cells significantly decreased cell migration and invasion. Furthermore, dual-luciferase analysis verified that PDCD4 was a direct target gene of miR-629 in NPC cells. Knockdown of PDCD4 in cells over-expressing miR-629 restored cell proliferation and metastasis.

CONCLUSIONS: In this study, the expression level of miR-629 was significantly increased in 83 NPC tissues and 4 cell lines. MiR-629 promoted NPC cell growth, migration, and invasion via repressing PDCD4 expression, which might provide a novel target for the future biotherapy for NPC.

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