Long noncoding RNA UCA1 promotes the proliferation, invasion, and migration of nasopharyngeal carcinoma cells via modulation of miR-145
Authors Wu J, Du M, Zhang Q, Zhang W, Fan Y, Yin L, Fei Q, Jiang X, Chen W, Zhu H, Yan P, He X, Bian X
Received 2 August 2018
Accepted for publication 28 September 2018
Published 25 October 2018 Volume 2018:11 Pages 7483—7492
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Carlos E Vigil
Jing Wu,1,* Mingyu Du,1,* Qian Zhang,1,* Wenjun Zhang,2 Yanxin Fan,1 Li Yin,1 Qian Fei,2 Xuesong Jiang,1 Wei Chen,1 Huanfeng Zhu,1 Pengwei Yan,1 Xia He,1 Xiuhua Bian1
1Department of Radiotherapy, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu, China; 2The Fourth Clinical Medical College of Nanjing Medical University, Nanjing, Jiangsu, China
*These authors contributed equally to this work
Background: Nasopharyngeal carcinoma (NPC) is a common malignant tumor characterized by highly malignant local invasion and distant metastasis. Recently, increasing attention has been paid to long noncoding RNAs (lncRNAs), which play significant roles in tumorigenesis and progression. However, little is known about the potential role of the lncRNA urothelial carcinoma-associated 1 (UCA1) in NPC cell invasion and migration.
Methods: Real-time quantitative PCR was used to analyze the expression of lncRNA UCA1 in NPC cell lines and NP69. lncRNA UCA1 knock-down nasopharyngeal carcinoma cell line models were established through siRNA. Cell viability was evaluated by Cell counting kit-8 and Colony forming assay. The migration and invasion capacities were evaluated by wound healing and transwell migration and invasion assays. Western blot analysis were used to examine protein changes followed by UCA1 knock-down.
Results: Our study confirmed that UCA1 was upregulated in NPC cell lines and involved in NPC tumorigenesis according to our established UCA1-associated competing endogenous RNA network. Moreover, functional analyses indicated that the downregulation of UCA1 exerted inhibitory effects on cell proliferation, invasion, and migration. Mechanistic analyses revealed that UCA1 was the target of miR-145 and functioned as a sponge to repress miR-145 expression. Rescue experiments suggested that lncRNA UCA1 reversed the miR-145-mediated inhibition on oncogene ADAM17 expression, thus promoting the proliferation, invasion, and migration of NPC cells.
Conclusion: LncRNA UCA1 functions as a tumor promoter in NPC. UCA1 promotes the proliferation and invasion of NPC cells by sponging miR-145, functionally altering ADAM17 expression targeted by miR-145. Our exploration of the underlying mechanism of UCA1 in NPC may provide novel therapeutic targets for NPC.
Keywords: NPC, UCA1, miR-145, proliferation, invasion, migration
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