LINC00152 promotes the growth and invasion of oral squamous cell carcinoma by regulating miR-139-5p
Authors Li M, Ning J, Li Z, Wang J, Zhao C, Wang L
Received 21 March 2018
Accepted for publication 26 May 2018
Published 27 September 2018 Volume 2018:11 Pages 6295—6304
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Samir Farghaly
Minghe Li,1,2 Jun Ning,3 Zhihong Li,4 Jing Wang,5 Cong Zhao,5 Lei Wang6
1Department of Oral and Maxillofacial Surgery, School of Stomatology Hospital of Jilin University, Changchun, China; 2Key Laboratory of Tooth Development and Bone Remodeling, School of Stomatology Jilin University, Changchun, China; 3Department of Gynaecology II, The First Hospital of Jilin University, Changchun, China; 4Department of Thoracic Surgery, The First Hospital of Jilin University, Changchun, China; 5Department of Endodontics, School of Stomatology Hospital of Jilin University, Changchun, China; 6Department of Periodontology, School of Stomatology Hospital of Jilin University, Changchun, China
Background: LINC00152 plays a crucial role in tumorigenesis and progression of multiple types of cancer. However, the biological significance of LINC00152 and its potential role in oral squamous cell carcinoma (OSCC) remain to be determined. In the present study, we investigated the role of LINC00152 and the underlying mechanism of its oncogenic activity in OSCC.
Materials and methods: The expression of LINC00152 in OSCC tissues and cell lines was detected using qRT-PCR. Cell proliferation, colony formation, migration, and invasion were measured using a cell counting kit, colony formation assay, wound healing, and transwell invasion assays, respectively. The target gene of LINC00152 was confirmed using a dual-luciferase reporter assay and qRT-PCR. A nude mouse model was established to analyze the function of LINC00152 in vivo.
Results: LINC00152 expression was significantly upregulated in OSCC tissues and cell lines compared with that in normal counterparts. Upregulated LINC00152 served as an independent prognostic predictor in patients with OSCC. Moreover, knockdown of LINC00152 inhibited cell proliferation, colony formation, migration, and invasion, and suppressed the epithelial to mesenchymal transition in vitro, as well as impairing tumor growth in vivo. A mechanistic investigation indicated that LINC00152 could directly bind to miR-139-5p in OSCC. LINC00152 expression was inversely correlated with miR-139 expression in OSCC tissues.
Conclusion: Taken together, these results suggested that LINC00152 may function as oncogene in OSCC and could be a potential therapeutic target in patients with OSCC.
Keywords: lncRNA, LINC00152, miR-139-5p, oral squamous cell carcinoma
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