Functions of microRNA-143 in the apoptosis, invasion and migration of nasopharyngeal carcinoma

被引:18
作者
Chen, Jin-Hui [1 ]
Yang, Rui [1 ]
Zhang, Wei [1 ]
Wang, Yong-Ping [1 ]
机构
[1] Wuhan Univ, Renmin Hosp, Dept Otorhinolaryngol Head & Neck Surg, 238 Jiefang Rd, Wuhan 430060, Hubei, Peoples R China
关键词
nasopharyngeal carcinoma; miR-143; apoptosis; metastasis; tumor suppressor; TUMOR-SUPPRESSOR; PROMOTES APOPTOSIS; TARGETING KRAS; MIR-143; CANCER; CELLS; IDENTIFICATION; PROLIFERATION; OSTEOSARCOMA; METASTASIS;
D O I
10.3892/etm.2016.3847
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Nasopharyngeal carcinoma (NPC) is a common cancer characterized by poor prognosis in areas of Southern China where it is endemic. microRNAs (miRNAs) are a class of naturally occurring small noncoding RNAs, some of which contribute to the initiation and development of cancer. The current study was designed to examine the expression level of miR-143 in NPC tissues. The potential functional targets of miR-143 involved in tumor apoptosis, invasion and migration were also investigated. Reverse transcription-quantitative polymerase chain reaction was used to evaluate the expression levels of miR-143 in clinical NPC specimens. Western blotting was used to explore the expression levels of extracellular signal regulated kinase (ERK)-5, Kirsten rat sarcoma viral oncogene homolog (KRAS), caspase 3 and B-cell lymphoma 2 (Bcl-2) in CNE-2Z cells following transfection with miR-143. Significantly decreased expression levels of miR-143 were observed in NPC tissues in comparison with matched normal nasopharyngeal tissues. Moreover, negative associations of miR-143 with tumor invasion depth, as well as lymph node metastasis were found. The enforced expression of miR-143 induced NPC cell apoptosis in addition to the suppression of growth, migration and invasion. The functions of miR-143 in NPC are mediated, at least in part, by the inhibition of ERK-5 activity and promotion of caspase 3 and KRAS expression. These findings suggest that miR-143 may function as a tumor suppressor in the development and progression of NPC.
引用
收藏
页码:3749 / 3755
页数:7
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