MicroRNA‑223‑5p suppresses the progression of nasopharyngeal carcinoma by targeting DCLK1

Abstract

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.

E74-like ETS transcription factor 1 promotes the progression of pancreatic cancer by regulating doublecortin-like kinase 1/Janus kinase/signal transducer and activator of transcription pathway

“…DCLK1 is a transmembrane microtubule-associated protein kinase with a DCX domain and a C-terminal serine/threonine protein kinase domain, which is considered to be a crucial modulator of cell movement [30]. Previous studies have shown that DCLK1 is highly expressed in a variety of cancers and has been identified as a potential oncogene associated with cancer progression, in intestinal tumor, non-small cell lung cancer and nasopharyngeal carcinoma [31][32][33][34]. In addition, there are a large number of reports about the role of DCLC1 in PC.…”