Long noncoding RNA NEAT1 promotes nasopharyngeal carcinoma progression through regulation of miR-124/NF-κB pathway.
Long noncoding RNA NEAT1 promotes nasopharyngeal carcinoma progression through regulation of miR-124/NF-κB pathway.
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DOI：
10.2147/ott.s151800
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发表时间：
2017
影响因子：
4
通讯作者：
Guo Y
中科院分区：
文献类型：
--
作者：
Cheng N;Guo Y
鼻咽癌（NPC）是最常见的恶性肿瘤之一，严重危害人们的健康。最近，长非编码RNA（lncRNA）NEAT1已被确定为多种癌症的致癌基因。然而，NEAT1在NPC中的作用及其潜在机制尚未得到很好的阐述。在这项研究中，数据显示鼻咽癌组织和细胞中 NEAT1 上调，miR-124 下调。功能丧失表明，NEAT1 敲低会抑制鼻咽癌细胞的增殖并促进其凋亡，而功能获得则表明，上调 NEAT1 则表现出相反的效果。此外，NEAT1 被证明可以通过与 NPC 细胞的直接相互作用来抑制 miR-124 的表达。此外，miR-124 逆转了 NEAT1 介导的促增殖和抗凋亡作用。此外，miR-124通过NF-κB信号通路调节NPC细胞增殖和凋亡。 NPC 小鼠模型证实 NEAT1 过表达通过调节体内 miR-124 促进肿瘤生长。综上所述，本研究表明，上调的 NEAT1 通过调节 miR-124/NF-κB 信号通路促进鼻咽癌的肿瘤发生和进展，这为鼻咽癌患者提供了一个有吸引力的治疗靶点。
Nasopharyngeal carcinoma (NPC) is one of the most common malignancies and seriously endangers people’s health. Recently, long noncoding RNA (lncRNA) NEAT1 has been determined as an oncogenic gene in a variety of cancers. However, the effect of NEAT1 in NPC and its underlying mechanism have not been well elaborated. In this study, the data showed that NEAT1 was upregulated and miR-124 was downregulated in NPC tissues and cells. Loss-of-function revealed that NEAT1 knockdown inhibited proliferation and promoted apoptosis of NPC cells while gain-of-function revealed that upregulated NEAT1 showed an opposite effect. Moreover, NEAT1 was demonstrated to suppress miR-124 expression by direct interaction in NPC cells. Additionally, miR-124 reversed NEAT1-mediated pro-proliferation and anti-apoptosis effect. Furthermore, miR-124 regulated NPC cell proliferation and apoptosis via NF-κB signal pathway. Mouse models of NPC confirmed that NEAT1 overexpression facilitated tumor growth by modulating miR-124 in vivo. Taken together, this study indicated that upregulated NEAT1 promoted the tumorigenesis and progression of NPC through regulating miR-124/NF-κB signaling pathway, suggesting an attractive therapy target for NPC patients.