Ye Chen1, Yiying Ding2. 1. Department of Stomatology, The Affiliated Hanyang Hospital of Wuhan University of Science and Technology, Wuhan, China. 2. Department of Outpatient Service, the Affiliated Hanyang Hospital of Wuhan University of Science and Technology, Wuhan, China.
Abstract
BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) has attracted the attention of researchers as a result of its high incidence around the world. This malignancy occurs in the oral cavity, pharynx and larynx in most cases. A number of lncRNAs have been revealed to regulate the malignant neoplasia of several cancers. Nevertheless, the effects of lncRNA LINC00467 in HNSCC have not yet been reported. METHODS: The expression of LINC00467, miR-299-5p and ubiquitin specific protease-48 (USP48) in HNSCC cells was quantified by a quantitative reverse transcriptase-polymerase chain reaction. The influences of LINC00467 deficiency on HNSCC progression were reflected by cell counting kit-8, colony formation, ethynyl-2-deoxyuridine, wound healing and western blot assays. RIP and luciferase reporter assays were conducted to confirm the interaction among LINC00467, miR-299-5p and USP48. RESULTS: LINC00467 was considerably upregulated in HNSCC cells, and an absence of LINC00467 suppressed cell growth, cell migration and the epithelial-mesenchymal process in HNSCC. In addition, miR-299-5p expression was notably downregulated in HNSCC cells, and miR-299-5p could bind with LINC00467. Furthermore, USP48 was conspicuously overexpressed in HNSCC cells and capable of binding with miR-299-5p. LINC00467 could upregulate USP48 expression via sponging miR-299-5p. Finally, rescue assays proved that USP48 overexpression could compensate for the suppressive effects on HNSCC progression mediated by LINC00467 deficiency. CONCLUSIONS: LINC00467 enhances HNSCC progression by serving as a sponge of miR-299-5p to increase USP48 expression.
BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) has attracted the attention of researchers as a result of its high incidence around the world. This malignancy occurs in the oral cavity, pharynx and larynx in most cases. A number of lncRNAs have been revealed to regulate the malignant neoplasia of several cancers. Nevertheless, the effects of lncRNA LINC00467 in HNSCC have not yet been reported. METHODS: The expression of LINC00467, miR-299-5p and ubiquitin specific protease-48 (USP48) in HNSCC cells was quantified by a quantitative reverse transcriptase-polymerase chain reaction. The influences of LINC00467 deficiency on HNSCC progression were reflected by cell counting kit-8, colony formation, ethynyl-2-deoxyuridine, wound healing and western blot assays. RIP and luciferase reporter assays were conducted to confirm the interaction among LINC00467, miR-299-5p and USP48. RESULTS:LINC00467 was considerably upregulated in HNSCC cells, and an absence of LINC00467 suppressed cell growth, cell migration and the epithelial-mesenchymal process in HNSCC. In addition, miR-299-5p expression was notably downregulated in HNSCC cells, and miR-299-5p could bind with LINC00467. Furthermore, USP48 was conspicuously overexpressed in HNSCC cells and capable of binding with miR-299-5p. LINC00467 could upregulate USP48 expression via sponging miR-299-5p. Finally, rescue assays proved that USP48 overexpression could compensate for the suppressive effects on HNSCC progression mediated by LINC00467 deficiency. CONCLUSIONS:LINC00467 enhances HNSCC progression by serving as a sponge of miR-299-5p to increase USP48 expression.