Department of Otorhinolaryngology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Eur Rev Med Pharmacol Sci. 2019 Jan;23(1):207-216. doi: 10.26355/eurrev_201901_16766.
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.
目的：microRNAs (miRNA) 已被证明参与了多种肿瘤的发生和发展，包括鼻咽癌 (NPC)。然而，miR-629 在 NPC 中的表达和功能尚未阐明。在这里，我们探讨了 miR-629 在 NPC 细胞中的作用，并研究了可能的潜在机制。
材料和方法：首先利用定量实时聚合酶链反应 (qRT-PCR) 检测 NPC 组织及相邻正常样本、NPC 细胞系和正常鼻咽细胞系 NP69 中 miR-629 的表达。在 NPC 细胞中转染 miR-629 模拟物和抑制剂，上调或下调 miR-629 的表达。MTT（3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐）检测和流式细胞术分别用于研究 miR-629 对已建立的 NPC 细胞增殖和细胞周期的影响。Transwell Matrigel 检测和划痕愈合检测用于评估细胞侵袭和迁移能力。同时，利用生物信息学预测和双荧光素酶分析检测 miR-629 在 NPC 中的潜在机制。此外，采用 Western blot 检测 miR-629 靶向蛋白的表达。
结果：miR-629 在 NPC 组织中的表达明显高于相邻正常样本。NPC 细胞中 miR-629 的表达明显高于 NP69 细胞。与阴性对照组相比，过表达 miR-629 可显著促进 6-10B 细胞增殖，而敲低 miR-629 可显著抑制 5-8F 细胞生长。miR-629 模拟物转染可显著增加细胞迁移和侵袭能力。然而，miR-629 抑制剂转染可显著降低细胞迁移和侵袭能力。此外，双荧光素酶分析证实 PDCD4 是 NPC 细胞中 miR-629 的直接靶基因。在过表达 miR-629 的细胞中敲低 PDCD4 可恢复细胞增殖和转移。
结论：本研究发现 miR-629 在 83 例 NPC 组织和 4 种细胞系中的表达水平明显升高。miR-629 通过抑制 PDCD4 表达促进 NPC 细胞生长、迁移和侵袭，这可能为 NPC 的未来生物治疗提供新的靶点。
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