M-Y Xue1, H-X Cao. 1. Department of Otorhinolaryngology-Head and Neck Surgery, Affiliated Hospital of Jiangnan University (The Fourth People's Hospital of Wuxi), Wuxi, China. yzchx@vip.163.com.
Abstract
OBJECTIVE: Nasopharyngeal carcinoma (NPC) is one of the most common malignant tumors worldwide. Recent studies have revealed that long non-coding RNAs (lncRNAs) play important roles in the progression of tumorigenesis. The aim of this study was to identify the exact role of lncRNA CASC15 in the progression of NPC. PATIENTS AND METHODS: CASC15 expression in both 54 paired NPC patients' tissue samples and cell lines was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Moreover, the function of CASC15 was identified by performing cell proliferation assay, transwell assay and wound healing assay in vitro. The underlying mechanism was explored through Luciferase assay and RT-qPCR. In addition, tumor formation and metastasis assays were conducted in vivo. RESULTS: CASC15 expression in NPC tissues was markedly higher than that of adjacent non-tumor tissues. The proliferation, migration and invasion of NPC cells were significantly inhibited after knockdown of CASC15 in vitro. Our further experiments revealed that miR-101-3p was remarkably up-regulated via knockdown of CASC15. Meanwhile, miR-101-3p was a direct target of CASC15 in NPC. Furthermore, tumor formation and metastasis of NPC were significantly inhibited via knockdown of CASC15 in nude mice. CONCLUSIONS: CASC15 enhances NPC cell proliferation and metastasis via sponging miR-101-3p in vitro and in vivo.
OBJECTIVE: Nasopharyngeal carcinoma (NPC) is one of the most common malignant tumors worldwide. Recent studies have revealed that long non-coding RNAs (lncRNAs) play important roles in the progression of tumorigenesis. The aim of this study was to identify the exact role of lncRNA CASC15 in the progression of NPC. PATIENTS AND METHODS: CASC15 expression in both 54 paired NPCpatients' tissue samples and cell lines was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Moreover, the function of CASC15 was identified by performing cell proliferation assay, transwell assay and wound healing assay in vitro. The underlying mechanism was explored through Luciferase assay and RT-qPCR. In addition, tumor formation and metastasis assays were conducted in vivo. RESULTS:CASC15 expression in NPC tissues was markedly higher than that of adjacent non-tumor tissues. The proliferation, migration and invasion of NPC cells were significantly inhibited after knockdown of CASC15 in vitro. Our further experiments revealed that miR-101-3p was remarkably up-regulated via knockdown of CASC15. Meanwhile, miR-101-3p was a direct target of CASC15 in NPC. Furthermore, tumor formation and metastasis of NPC were significantly inhibited via knockdown of CASC15 in nude mice. CONCLUSIONS:CASC15 enhances NPC cell proliferation and metastasis via sponging miR-101-3p in vitro and in vivo.