microRNA-124 inhibits stem-like properties and enhances radiosensitivity in nasopharyngeal carcinoma cells via direct repression of expression of JAMA

被引:15
作者
Tian, Yunhong [1 ]
Tian, Yunming [2 ]
Tu, Yinuo [1 ]
Zhang, Guoqian [1 ]
Zeng, Xing [1 ]
Lin, Jie [1 ]
Ai, Meiling [1 ]
Mao, Zixu [3 ]
Zheng, Ronghui [1 ]
Yuan, Yawei [1 ]
机构
[1] Guangzhou Med Univ, Affiliated Canc Hosp & Inst, State Key Lab Resp Dis, Guangzhou, Peoples R China
[2] Hui Zhou Municipal Cent Hosp, Dept Radiat Oncol, Huizhou, Peoples R China
[3] Emory Univ, Sch Med, Dept Pharmacol & Chem Biol, Atlanta, GA USA
基金
中国国家自然科学基金;
关键词
junctional adhesion molecule A; microRNA-124; nasopharyngeal carcinoma; stem-like properties; EPITHELIAL-MESENCHYMAL TRANSITION; JUNCTIONAL ADHESION MOLECULE; DIFFERENTIATION; METASTASIS; POPULATION; MIGRATION; MARKER;
D O I
10.1111/jcmm.15177
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cancer stem cells (CSCs) are a source of tumour recurrence in patients with nasopharyngeal carcinoma (NPC); however, the function of microRNA-124 (miR-124) in NPC CSCs has not been clearly defined. In this study, we investigated the role of miR-124 in NPC CSCs. qRT-PCR was performed to measure miR-124 expression in NPC tissues and cell lines and the effects of miR-124 on stem-like properties and radiosensitivity of NPC cells measured. Luciferase reporter assays and rescue experiments were used to investigate the interaction of miR-124 with the 3 ' UTR of junctional adhesion molecule A (JAMA). Finally, we examined the effects of miR-124 in an animal model and clinical samples. Down-regulation of miR-124 was detected in cancer tissues and was inversely associated with tumour stage and lymph node metastasis. Overexpression of miR-124 inhibited stemness properties and enhanced radiosensitivity of NPC cells in vitro and in vivo via targeting JAMA. Up-regulation of miR-124 was correlated with superior overall survival of patients with NPC. Our study demonstrates that miR-124 can inhibit stem-like properties and enhance radiosensitivity by directly targeting JAMA in NPC. These findings provide novel insights into the molecular mechanisms underlying therapy failure in NPC.
引用
收藏
页码:9533 / 9544
页数:12
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