Xingkai Ma1, Yifang Yuan1, Jianbin Lu1, Menglin Li1, Yan Yu1, Jianyong Liu2, Jieyu Zhou3. 1. Department of Otorhinolaryngology, Zhangjiagang First People's Hospital, Affiliated Hospital of Soochow University, Suzhou 215600, Jiangsu, China. 2. Department of Otorhinolaryngology, Zhangjiagang First People's Hospital, Affiliated Hospital of Soochow University, Suzhou 215600, Jiangsu, China. Electronic address: zjgljyys@163.com. 3. Department of Otolaryngology-Head and Neck Surgery, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 201999, China; Ear Institute Shanghai Jiaotong University School of Medicine, Shanghai Key Laboratory of Translational Medicine on Ear and Nose Diseases, Shanghai 200025, China. Electronic address: entzhoujieyu@hotmail.com.
Abstract
BACKGROUND: In 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. METHODS: RT-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. RESULTS: ANCR 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. CONCLUSIONS: Long noncoding RNA ANCR suppresses malignant behaviors of nasopharyngeal carcinoma cells by regulating miR-4731-5p/NMT1 axis.
BACKGROUND: In 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. METHODS: RT-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. RESULTS: ANCR 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. CONCLUSIONS: Long noncoding RNA ANCR suppresses malignant behaviors of nasopharyngeal carcinoma cells by regulating miR-4731-5p/NMT1 axis.