Bo Jia1,2, Junfeng Dao3, Jiusong Han2, Zhijie Huang2, Xiang Sun2, Xianghuai Zheng2, Shijian Xiang4, Huixi Zhou5, Shuguang Liu6. 1. Department of Stomatology, Shunde Hospital, Southern Medical University, Foshan, Guangdong, 528300, China. 2. Department of Oral Surgery, Stomatological Hospital, Southern Medical University, Guangzhou, 510280, China. 3. Department of Prosthodontics, Stomatological Hospital, Southern Medical University, Guangzhou, 510280, China. 4. Department of Pharmacy, Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, 518107, China. 5. Department of Oral Surgery, Stomatological Hospital, Southern Medical University, Guangzhou, 510280, China. zhouhuixikqwk@163.com. 6. Department of Oral Surgery, Stomatological Hospital, Southern Medical University, Guangzhou, 510280, China. liushuguangwk@163.com.
Abstract
BACKGROUND: Tongue squamous cell carcinoma (TSCC) is one of the most common oral tumors. Recently, long intergenic noncoding RNA 00958 (LINC00958) has been identified as an oncogene in human cancers. Nevertheless, the role of LINC00958 and its downstream mechanisms in TSCC is still unknown. METHODS: The effect of LINC00958 on TSCC cells proliferation and growth were assessed by CCK-8, colony formation, 5-Ethynyl-2'-deoxyuridline (EdU) assay and flow cytometry assays in vitro and tumor xenograft model in vivo. Bioinformatics analysis was used to predict the target of LINC00958 in TSCC, which was verified by RNA immunoprecipitation and luciferase reporter assays. RESULTS: LINC00958 was increased in TSCC tissues, and patients with high LINC00958 expression had a shorter overall survival. LINC00958 knockdown significantly decreased the growth rate of TSCC cells both in vitro and in vivo. In mechanism, LINC00958 acted as a ceRNA by competitively sponging miR-211-5p. In addition, we identified CENPK as a direct target gene of miR-211-5p, which was higher in TSCC tissues than that in adjacent normal tissues. Up-regulated miR-211-5p or down-regulated CENPK could abolish LINC00958-induced proliferation promotion in TSCC cells. Furthermore, The overexpression of CENPK promoted the expression of oncogenic cell cycle regulators and activated the JAK/STAT3 signaling. CONCLUSIONS: Our findings suggested that LINC00958 is a potential prognostic biomarker in TSCC.
BACKGROUND:Tongue squamous cell carcinoma (TSCC) is one of the most common oral tumors. Recently, long intergenic noncoding RNA 00958 (LINC00958) has been identified as an oncogene in humancancers. Nevertheless, the role of LINC00958 and its downstream mechanisms in TSCC is still unknown. METHODS: The effect of LINC00958 on TSCC cells proliferation and growth were assessed by CCK-8, colony formation, 5-Ethynyl-2'-deoxyuridline (EdU) assay and flow cytometry assays in vitro and tumor xenograft model in vivo. Bioinformatics analysis was used to predict the target of LINC00958 in TSCC, which was verified by RNA immunoprecipitation and luciferase reporter assays. RESULTS:LINC00958 was increased in TSCC tissues, and patients with high LINC00958 expression had a shorter overall survival. LINC00958 knockdown significantly decreased the growth rate of TSCC cells both in vitro and in vivo. In mechanism, LINC00958 acted as a ceRNA by competitively sponging miR-211-5p. In addition, we identified CENPK as a direct target gene of miR-211-5p, which was higher in TSCC tissues than that in adjacent normal tissues. Up-regulated miR-211-5p or down-regulated CENPK could abolish LINC00958-induced proliferation promotion in TSCC cells. Furthermore, The overexpression of CENPK promoted the expression of oncogenic cell cycle regulators and activated the JAK/STAT3 signaling. CONCLUSIONS: Our findings suggested that LINC00958 is a potential prognostic biomarker in TSCC.