OncoTargets and Therapy | |
MicroRNA-92a promotes metastasis of nasopharyngeal carcinoma by targeting the PTEN/AKT pathway | |
关键词: MicroRNA-92a; Nasopharyngeal carcinoma; PTEN; Signaling pathway; Tumor metastasis; | |
DOI : | |
来源: DOAJ |
【 摘 要 】
Haixiong Zhang,1 Hui Cao,1 Dadao Xu,1 Kang Zhu21Department of Otorhinolaryngology, Head and Neck Surgery, the First Affiliated Hospital of Xi’an Medical College, 2Department of Otorhinolaryngology, Head and Neck Surgery, the Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, People’s Republic of ChinaAbstract: 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.Keywords: microRNA-92a, nasopharyngeal carcinoma, PTEN, signaling pathway, tumor metastasis, non-coding RNA, head and neck neoplasms
【 授权许可】
Unknown