RETRACTED: Long noncoding RNA NEAT1 promotes nasopharyngeal carcinoma progression through regulation of miR-124/NF-κB pathway (Retracted article. See vol. 16, pg. 639, 2023)

被引:57
作者
Cheng, Nan [1 ]
Guo, Yang [2 ]
机构
[1] Henan Univ, Huaihe Hosp, Dept Otolaryngol, 8 Baobei Rd, Kaifeng 475000, Peoples R China
[2] Kaifeng Cent Hosp, Kaifeng Eye Hosp, Dept Ophthalmol, Kaifeng, Peoples R China
关键词
nasopharyngeal carcinoma; lncRNA; NEAT1; miR-124; NF-kappa B pathway; CELL LUNG-CANCER; KAPPA-B PATHWAY; MESENCHYMAL TRANSITION; INVASION; PROLIFERATION; METASTASIS; MIGRATION; GROWTH; MICRORNAS; AXIS;
D O I
10.2147/OTT.S151800
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
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-kappa B 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-kappa B signaling pathway, suggesting an attractive therapy target for NPC patients.
引用
收藏
页码:5843 / 5853
页数:11
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