Zhang Shasha, Xu Meiai, Shen Xuefeng, Jiang Sicong, He Xianming, Ke Juying
Department of Otolaryngology, Sanmen People's Hospital.
Division of Thoracic and Endocrine Surgery, University Hospitals and University of Geneva.
Tohoku J Exp Med. 2025 Aug 21;266(4):353-360. doi: 10.1620/tjem.2024.J131. Epub 2024 Nov 7.
Nasopharyngeal carcinoma (NPC) is a serious malignancy occurring in nasopharynx with high incidence, which is caused by excessive proliferation of nasopharyngeal cells. It has been reported that both microRNA (miR)-616-5p and glycogen synthase kinase 3β (GSK3β) are involved in multiple biological processes in various cancer cells and there is a targeting relationship between them. However, their roles in NPC remain undiscovered. This study was to investigate the prognosis and regulatory role of miR-616-5p/ GSK3β in NPC. 136 patients with NPC were enrolled and provided tissue samples. The NPC cell line SUNE-1 was used to explore the effect of miR-616-5p on NPC. Cell transfection was used to regulate gene expression and the expression levels of miR-616-5p and GSK3β were confirmed by qRT-PCR. Results confirmed that miR-616-5p was increased in both NPC tissues of patients and NPC cell lines. Further Kaplan-Meier assay showed that increased miR-616-5p was related to the poor prognosis of NPC patients. Subsequent assessment on cellular biological behavior demonstrated that up-regulated miR-616-5p facilitated cell proliferation, migration and invasion while it suppressed cell apoptosis. In addition, GSK3β was identified as a potential downstream target of miR-616-5p by dual-luciferase system. In conclusion, up-regulated miR-616-5p may promote the progression of NPC via targeting GSK3β.
鼻咽癌(NPC)是一种发生于鼻咽部的严重恶性肿瘤,发病率高,由鼻咽细胞过度增殖引起。据报道,微小RNA(miR)-616-5p和糖原合酶激酶3β(GSK3β)均参与多种癌细胞的多个生物学过程,且它们之间存在靶向关系。然而,它们在鼻咽癌中的作用仍未被发现。本研究旨在探讨miR-616-5p/GSK3β在鼻咽癌中的预后及调控作用。招募了136例鼻咽癌患者并提供了组织样本。使用鼻咽癌细胞系SUNE-1来探究miR-616-5p对鼻咽癌的影响。采用细胞转染来调节基因表达,并通过qRT-PCR确认miR-616-5p和GSK3β的表达水平。结果证实,miR-616-5p在鼻咽癌患者组织和鼻咽癌细胞系中均升高。进一步的Kaplan-Meier分析表明,miR-616-5p升高与鼻咽癌患者预后不良相关。随后对细胞生物学行为的评估表明,上调miR-616-5p促进细胞增殖、迁移和侵袭,同时抑制细胞凋亡。此外,通过双荧光素酶系统确定GSK3β为miR-616-5p的潜在下游靶点。总之,上调的miR-616-5p可能通过靶向GSK3β促进鼻咽癌的进展。