Nasopharyngeal carcinoma (NPC) is a major otorhinolaryngological disease with limited effective therapeutic options. This work focused on the function of microRNA-384 (miR-384) on the NPC pathogenesis and the molecules involved. miR-384 expression in cancer tissues and cells was detected. Gain- and loss-of-functions of miR-384 were performed to identify its role in NPC progression. The target mRNA of miR-384 was predicted on an online system and validated through a luciferase reporter assay. The activity of Wnt/β-catenin signaling was detected. Consequently, miR-384 was found to be poorly expressed in NPC tissues and cell lines and was linked to unfavorable survival rates in patients. Overexpression of miR-384 in 6-10B cells suppressed growth, migration, invasion and resistance to apoptosis of cells, but inverse trends were presented in C6661 cells where miR-384 was downregulated. miR-384 targeted Smad5 mRNA. Upregulation of Smad5 counteracted the roles of miR-384 mimic in cells. The NPC-inhibiting effects of miR-384 mimic were also blocked by Wnt/β-catenin activation. To conclude, miR-384 targets Smad5 and inactivates the Wnt/β-catenin pathway, which exerts a suppressing role in NPC cell behaviors as well as tumor growth in vivo. The findings may offer novel thoughts into NPC therapy.

鼻咽癌（NPC）是一种主要的耳鼻喉科疾病，有效的治疗选择有限。这项工作的重点是 microRNA-384 (miR-384) 在 NPC 发病机制中的作用以及所涉及的分子。检测到miR-384在癌组织和细胞中的表达。进行了 miR-384 的功能获得和丧失，以确定其在 NPC 进展中的作用。在在线系统上预测 miR-384 的靶 mRNA，并通过荧光素酶报告基因测定进行验证。检测到 Wnt/β-catenin 信号的活性。因此，发现 miR-384 在 NPC 组织和细胞系中表达不佳，并且与患者的不利存活率有关。miR-384在6-10B细胞中的过表达抑制细胞的生长、迁移、侵袭和抗凋亡，但在 miR-384 下调的 C6661 细胞中呈现相反的趋势。miR-384 靶向 Smad5 mRNA。Smad5 的上调抵消了 miR-384 模拟物在细胞中的作用。miR-384 模拟物的 NPC 抑制作用也被 Wnt/β-连环蛋白激活所阻断。总之，miR-384 靶向 Smad5 并使 Wnt/β-catenin 通路失活，该通路在 NPC 细胞行为和体内肿瘤生长中发挥抑制作用。这些发现可能为 NPC 治疗提供新的思路。它在 NPC 细胞行为以及体内肿瘤生长中发挥抑制作用。这些发现可能为 NPC 治疗提供新的思路。它在 NPC 细胞行为以及体内肿瘤生长中发挥抑制作用。这些发现可能为 NPC 治疗提供新的思路。