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

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 ro...

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Published in:Pathology, research and practice Vol. 224; p. 153540
Main Authors: Ma, Xingkai, Yuan, Yifang, Lu, Jianbin, Li, Menglin, Yu, Yan, Liu, Jianyong, Zhou, Jieyu
Format: Journal Article
Language:English
Published: Germany Elsevier GmbH 01-08-2021
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Abstract 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. 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. 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. Long noncoding RNA ANCR suppresses malignant behaviors of nasopharyngeal carcinoma cells by regulating miR-4731-5p/NMT1 axis.
AbstractList 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. 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. 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. Long noncoding RNA ANCR suppresses malignant behaviors of nasopharyngeal carcinoma cells by regulating miR-4731-5p/NMT1 axis.
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.
ArticleNumber 153540
Author Liu, Jianyong
Yuan, Yifang
Ma, Xingkai
Zhou, Jieyu
Li, Menglin
Yu, Yan
Lu, Jianbin
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  organization: Department of Otolaryngology-Head and Neck Surgery, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 201999, China
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Keywords Nasopharyngeal carcinoma
NMT1
ANCR
MiR-4731-5p
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Snippet In our previous study, we revealed that Antidifferentiation noncoding RNA (ANCR) promoted proliferation and radiation resistance of nasopharyngeal carcinoma...
BACKGROUNDIn our previous study, we revealed that Antidifferentiation noncoding RNA (ANCR) promoted proliferation and radiation resistance of nasopharyngeal...
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StartPage 153540
SubjectTerms ANCR
Cell Line, Tumor
Cell Movement - genetics
Cell Proliferation - genetics
Epithelial-Mesenchymal Transition - genetics
Gene Expression Regulation, Neoplastic
Humans
MicroRNAs - genetics
MiR-4731-5p
Nasopharyngeal carcinoma
Nasopharyngeal Carcinoma - pathology
Nasopharyngeal Neoplasms - genetics
Nasopharyngeal Neoplasms - pathology
NMT1
RNA, Long Noncoding - genetics
Title Long noncoding RNA ANCR promotes migration, invasion, EMT progress and stemness of nasopharyngeal carcinoma cells via the miR-4731-5p/NMT1 axis
URI https://dx.doi.org/10.1016/j.prp.2021.153540
https://www.ncbi.nlm.nih.gov/pubmed/34333213
https://search.proquest.com/docview/2557543673
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