miR-331-3p 通过靶向 elf4B-PI3K-AKT 通路抑制鼻咽癌细胞增殖并促进其凋亡。
miR-331-3p Inhibits Proliferation and Promotes Apoptosis of Nasopharyngeal Carcinoma Cells by Targeting elf4B-PI3K-AKT Pathway.
机构信息
Department of Radiotherapy, Dongguan People' Hospital, Dongguan, China.
Department of Medical Oncology, Dongguan People' Hospital, Dongguan, Guangdong, China.
出版信息
Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033819892251. doi: 10.1177/1533033819892251.
BACKGROUND
The incidence of nasopharyngeal carcinoma is increasing gradually, but the pathogenesis is not completely clear. MicroRNA, a highly conserved endogenous noncoding small molecule RNA, plays an essential role in the regulation of gene expression and is a hotspot in cancer research worldwide.
OBJECTIVES
Although previous studies have confirmed that the abnormal expression of microRNAs is closely related to the progression of nasopharyngeal carcinoma, the role of miRNA-331-3p in nasopharyngeal carcinoma has not been studied. The purpose of this study was to explore the role and mechanism of miRNA-331-3p in the progression of nasopharyngeal carcinoma.
MATERIALS AND METHODS
Real-time quantitative reverse transcription polymerase chain reaction was performed to detect the expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cell lines (CNE-1 and 5-8F cells). After overexpression of miRNA-331-3p in CNE-1 cells, cell proliferation was measured by Cell Counting Kit-8 assay, cell invasion was detected by Transwell assay, and apoptosis was tested by flow cytometry. In addition, the dual-luciferase reporter assay was used to identify the target gene of miRNA-331-3p and Western blotting was performed to measure the relative protein expression.
RESULTS
The expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cells was decreased significantly. Overexpression of miRNA-331-3p markedly inhibited the proliferation and invasion of CNE-1 cells and promoted cell apoptosis. Moreover, overexpression of miRNA-331-3p reduced the expression of target gene elF4B, leading to inhibition of the phosphorylation of Phosphoinositide 3-kinase (PI3K) and Serine/ threonine kinase (AKT).
CONCLUSION
miRNA-331-3p inhibited cell proliferation and induced cell apoptosis in nasopharyngeal carcinoma by targeting gene and then blocked the PI3K-AKT signaling pathway.
SIGNIFICANCE
The role of miRNA-331-3p in the development of NPC and its mechanism provide new ideas for the treatment of nasopharyngeal carcinoma.
背景
鼻咽癌的发病率逐渐增高，但发病机制尚不完全清楚。微小 RNA 是一种高度保守的内源性非编码小分子 RNA，在基因表达调控中发挥着重要作用，是目前癌症研究的热点。
目的
虽然已有研究证实微小 RNA 的异常表达与鼻咽癌的发生发展密切相关，但 miRNA-331-3p 在鼻咽癌中的作用尚不清楚。本研究旨在探讨 miRNA-331-3p 在鼻咽癌发生发展中的作用及其机制。
材料和方法
采用实时定量反转录聚合酶链反应检测鼻咽癌临床样本和细胞系（CNE-1 和 5-8F 细胞）中 miRNA-331-3p 的表达。在 CNE-1 细胞中转染过表达 miRNA-331-3p 后，通过细胞计数试剂盒-8 法检测细胞增殖，Transwell 小室法检测细胞侵袭，流式细胞术检测细胞凋亡。此外，采用双荧光素酶报告基因实验鉴定 miRNA-331-3p 的靶基因，Western blot 检测相关蛋白的相对表达。
结果
miRNA-331-3p 在鼻咽癌临床样本和细胞中的表达明显下调。过表达 miRNA-331-3p 可显著抑制 CNE-1 细胞的增殖和侵袭，促进细胞凋亡。此外，过表达 miRNA-331-3p 降低了靶基因 elF4B 的表达，从而抑制了磷酸肌醇 3-激酶（PI3K）和丝氨酸/苏氨酸激酶（AKT）的磷酸化。
结论
miRNA-331-3p 通过靶向基因抑制鼻咽癌细胞的增殖并诱导细胞凋亡，进而阻断 PI3K-AKT 信号通路。
意义
miRNA-331-3p 在 NPC 发生发展中的作用及其机制为鼻咽癌的治疗提供了新的思路。
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