Abstract
PURPOSE: The aberrant expression of long noncoding RNAs (lncRNAs) indicates progression of various diseases. LINC00958 has been well studied in several types of human cancer; however, the expression profile, functions, and potential mechanism of action of this lncRNA in nasopharyngeal carcinoma (NPC) remain largely unclear and still need to be elucidated. In the present study, we aimed to measure LINC00958 expression in NPC, determine its clinical value, and explore its roles in NPC progression as well as the mechanisms behind these processes. METHODS: The expression profile of LINC00958 in NPC was evaluated by reverse-transcription quantitative polymerase chain reaction (RT-qPCR). A series of functional assays, including the Cell Counting Kit-8 assay, flow cytometry, a Transwell assay, and an in vivo nude mouse model, were utilized to determine the participation of LINC00958 in the malignancy of NPC. RESULTS: LINC00958 was found to be upregulated in NPC tissue specimens and cell lines. The LINC00958 overexpression significantly correlated with tumor size, lymph node status, TNM stage, and worse overall survival among NPC patients. Downregulation of LINC00958 suppressed NPC cell proliferation, migration, and invasion and induced apoptosis in vitro. Additionally, the LINC00958 knockdown impaired tumor growth in vivo. Mechanistically, LINC00958 was found to serve as a molecular sponge of microRNA-625 (miR-625), thereby upregulating NUAK family SNF1-like kinase 1 (NUAK1) in NPC cells. Lastly, rescue experiments validated the involvement of the miR-625-NUAK1 axis in LINC00958-mediated biological functions in NPC. CONCLUSION: Our results demonstrated that LINC00958 works as an oncogene in NPC and plays a key role in the malignant phenotype of NPC cells by sponging miR-625 and increasing NUAK1 expression. The LINC00958-miR-625-NUAK1 pathway might be a target for anticancer therapy in patients with NPC.