MicroRNA-92a promotes metastasis of nasopharyngeal carcinoma by targeting the PTEN/AKT pathway

被引:37
|
作者
Zhang, Haixiong [1 ]
Cao, Hui [1 ]
Xu, Dadao [1 ]
Zhu, Kang [2 ]
机构
[1] Xian Med Coll, Affiliated Hosp 1, Dept Otorhinolaryngol Head & Neck Surg, Xian, Peoples R China
[2] Xi An Jiao Tong Univ, Affiliated Hosp 2, Dept Otorhinolaryngol Head & Neck Surg, 157 Xiwu Rd, Xian 710004, Peoples R China
来源
ONCOTARGETS AND THERAPY | 2016年 / 9卷
基金
中国国家自然科学基金;
关键词
microRNA-92a; nasopharyngeal carcinoma; PTEN; signaling pathway; tumor metastasis; non-coding RNA; head and neck neoplasms; HUMAN HEPATOCELLULAR-CARCINOMA; TUMOR-GROWTH; CELLS; CHEMORESISTANCE; EPIDEMIOLOGY; SURVIVAL; MIR-92A; CANCER; EMT;
D O I
10.2147/OTT.S105470
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
MicroRNAs have been confirmed to be a group of important regulators during the pathogenesis of nasopharyngeal carcinoma (NPC). This study confirmed that the expression of microRNA-92a (miR-92a) was significantly upregulated in NPC as compared to noncancerous nasopharyngeal epithelial tissues. Furthermore, high expression of miR-92a was observed in all NPC cell lines, especially in high metastatic cell lines. Clinical analysis indicated that high expression of miR-92a was associated with adverse clinicopathological features including the advanced tumor-node-metastasis stage and distant metastasis, and conferred poor prognosis of patients. In vitro assays showed that miR-92a overexpression potentiated the migration and invasion of 6-10B cells, and miR-92a silencing reduced the number of migrated and invaded 5-8F cells. Phosphatase and tensin homolog (PTEN) was confirmed as a direct downstream target of miR-92a in NPC cells. Otherwise, alteration of miR-92a expression regulated PTEN/AKT pathway in NPC cells. Mechanistically, miR-92a exerted its promoting effects on the metastatic behaviors of NPC cells through suppressing PTEN/AKT pathway. Taken together, this study demonstrates that miR-92a is a promising prognostic biomarker for patients with NPC, and may be a potential therapeutic target to prevent the metastasis of NPC.
引用
收藏
页码:3579 / 3588
页数:10
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