Long noncoding RNA ANCR promotes migration, invasion, EMT progress and stemness of nasopharyngeal carcinoma cells via the miR-4731-5p/NMT1 axis

Abstract

BackgroundIn our previous study, we revealed that Antidifferentiation noncoding RNA (ANCR) promoted proliferation and radiation resistance of nasopharyngeal carcinoma (NPC) cells. However, the molecular mechanism and function of ANCR are not fully studied. The current study aimed to further investigate the role and underlying molecular mechanism of ANCR in NPC. MethodsRT-qPCR and western blot analyses were used to detect the levels of RNAs and proteins in NPC cells. Wound healing and Transwell assays were used to examine the migration and invasion of NPC cells. The relationship among ANCR, miR-4731-5p and N-myristoyltransferase 1 (NMT1) was investigated by RIP and luciferase reporter assays. The NPC cell stemness was accessed by the sphere formation assay. ResultsANCR was significantly highly expressed in NPC cell lines. Silenced ANCR suppressed cell migration, invasion epithelial-mesenchymal transition (EMT) process and cell stemness in NPC. Furthermore, ANCR sponged miR-4731-5p to upregulate the NMT1 expression. Rescue assays indicated that NMT1 neutralized the antioncogenic effect induced by silenced ANCR on NPC cells. ConclusionsLong noncoding RNA ANCR suppresses malignant behaviors of nasopharyngeal carcinoma cells by regulating miR-4731-5p/NMT1 axis.