Zhang Zhixuan, Li Haifeng, You Jianqiang, Xue Haixiang, Tan Xiaoye, Chao Changjiang
Department of Otorhinolaryngology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213000, P.R. China.
Oncol Lett. 2021 May;21(5):396. doi: 10.3892/ol.2021.12657. Epub 2021 Mar 18.
The aim of the present study was to investigate the function of microRNA (miR)-223-5p in the malignant biological behavior of nasopharyngeal carcinoma (NPC) and elucidate the underlying molecular mechanism. The expression levels of miR-223-5p and doublecortin-like kinase 1 (DCLK1) were detected via reverse transcription-quantitative PCR analysis. Cell viability was evaluated using Cell Counting Kit-8 assay. Cell migration and invasion were measured via Transwell assays, while a luciferase reporter assay was conducted to identify the interaction between miR-223-5p and DCLK1. The results demonstrated that miR-223-5p expression was significantly downregulated, whereas DCLK1 expression was significantly upregulated in NPC tissues and cells. Moreover, both miR-223-5p overexpression and DCLK1 silencing markedly suppressed the progression of NPC. It was also observed that miR-223-5p directly targeted DCLK1 and decreased its expression. Furthermore, it was suggested that DCLK1 overexpression may partially reverse the suppressive effects of miR-223-5p on the progression of NPC. Collectively, the results of the present study indicated that miR-223-5p may suppress NPC progression by targeting DCLK1, thereby indicating a novel potential approach to the diagnosis and treatment of NPC.
本研究旨在探讨微小RNA（miR）-223-5p在鼻咽癌（NPC）恶性生物学行为中的作用，并阐明其潜在的分子机制。通过逆转录-定量聚合酶链反应分析检测miR-223-5p和双皮质素样激酶1（DCLK1）的表达水平。使用细胞计数试剂盒-8检测法评估细胞活力。通过Transwell检测法测量细胞迁移和侵袭能力，同时进行荧光素酶报告基因检测以确定miR-223-5p与DCLK1之间的相互作用。结果表明，在NPC组织和细胞中，miR-223-5p表达显著下调，而DCLK1表达显著上调。此外，miR-223-5p过表达和DCLK1沉默均显著抑制了NPC的进展。还观察到miR-223-5p直接靶向DCLK1并降低其表达。此外，提示DCLK1过表达可能部分逆转miR-223-5p对NPC进展的抑制作用。总体而言，本研究结果表明，miR-223-5p可能通过靶向DCLK1抑制NPC进展，从而为NPC的诊断和治疗指明了一种新的潜在方法。
