Affordable Access

deepdyve-link
Publisher Website

Long noncoding RNA cytoskeleton regulator RNA promotes cell invasion and metastasis by titrating miR-613 to regulate ANXA2 in nasopharyngeal carcinoma.

Authors
  • Chen, Wei1
  • Du, Mingyu1
  • Hu, Xinyu1
  • Ma, Hongxia2
  • Zhang, Erbao2
  • Wang, Tingting1
  • Yin, Li1
  • He, Xia1
  • Hu, Zhibin2
  • 1 Jiangsu Institute of Cancer Research, Jiangsu Cancer Hospital, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, China. , (China)
  • 2 Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Department of Epidemiology, Collaborative Innovation Center For Cancer Personalized Medicine, School of Public Health, Nanjing Medical University, Nanjing, China. , (China)
Type
Published Article
Journal
Cancer Medicine
Publisher
Wiley
Publication Date
Dec 20, 2019
Identifiers
DOI: 10.1002/cam4.2778
PMID: 31859457
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Nasopharyngeal carcinoma (NPC) is one of the most frequent head and neck malignant tumors. Long noncoding RNAs play critical roles in tumorigenesis. Real-time quantitative PCR arrays were used to evaluate the expression levels of cytoskeleton regulator RNA (CYTOR) in NPC tissues and cells. Cell counting kit-8 and colony formation analyses were used to test the NPC cell viability, while wound healing and transwell assays were employed to detect cell invasion and migration ability. Luciferase reporter assay and Western blot analyses were employed to explore the relationships among CYTOR, miR-613, and ANXA2. We found that CYTOR expression was elevated both in NPC tissues and cells. Functional assays revealed that CYTOR promoted the invasion and migration of NPC cells. The established spontaneous lymph node metastasis model also confirmed that CYTOR promoted NPC cell metastasis in vivo. Mechanically, we found that the subcellular localization of CYTOR mostly occurred in the cell cytoplasm. Luciferase reporter and RIP assays confirmed that CYTOR functioned as the molecular sponge of miR-613. Subsequent experiments confirmed that ANXA2 was directly targeted by miR-613. Gain- and loss-of-function studies further confirmed that CYTOR induced the upregulation of ANXA2 by competitively binding to miR-613, thus leading to NPC metastasis. Our results highlight the importance of CYTOR in NPC development and provide new insights into potential therapeutic targets for NPC. © 2019 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

Report this publication

Statistics

Seen <100 times