Bingyi Shao1, Xiaohui Fu2, Xian Li3, Yong Li3, Ning Gan1. 1. Department of Operative Dentistry and Endodontics, Stomatological Hospital of Chongqing Medical University, Chongqing, China. 2. Department of General Dentistry, The Second Affiliated Hospital of Zhejiang University, Hangzhou, China. 3. Department of Oral and Maxillofacial Surgery, Stomatological Hospital of Chongqing Medical University, Chongqing, China.
Abstract
BACKGROUND: Increasing evidence suggests that dysregulated long non-coding RNAs (lncRNAs) are involved in tumorigenesis and progression. RP11-284F21.9, one of the temporally expressed S-phase lncRNAs in cancer cells, was recently identified by nascent RNA capture sequencing. METHODS: Cal-27, Tca8113, SCC-9, HB56, and oral squamous cell carcinoma (OSCC) tissues were used in the experiment. RNA extraction, qRT-PCR, plasmid construction, cell proliferation, EdU labeling, Transwell migration, luciferase reporter, and western blotting were used to investigate the exact role and function of RP11-284F21.9 in cancer. RESULTS: RP11-284F21.9 was upregulated in human OSCC samples and cell lines. RP11-284F21.9 depletion suppressed the proliferation, migration, and invasion of OSCC cell lines. There was interaction between RP11-284F21.9, miR-383-5p, and MAL2. Increased MAL2 and decreased miR-383-5p expression were also detected in OSCC tissues and cell lines. In addition, RP11-284F21.9 knockdown could reduce MAL2 expression, while miR-383-5p inhibitors abolished this repressive effect. RP11-284F21.9 acted as a competing endogenous RNA (ceRNA) of miR-383-5p, leading to MAL2 upregulation, and subsequently promoted OSCC progression. CONCLUSION: RP11-284F21.9/miR-383-5p represents a novel and potential therapeutic target for the treatment of OSCC.
BACKGROUND: Increasing evidence suggests that dysregulated long non-coding RNAs (lncRNAs) are involved in tumorigenesis and progression. RP11-284F21.9, one of the temporally expressed S-phase lncRNAs in cancer cells, was recently identified by nascent RNA capture sequencing. METHODS: Cal-27, Tca8113, SCC-9, HB56, and oral squamous cell carcinoma (OSCC) tissues were used in the experiment. RNA extraction, qRT-PCR, plasmid construction, cell proliferation, EdU labeling, Transwell migration, luciferase reporter, and western blotting were used to investigate the exact role and function of RP11-284F21.9 in cancer. RESULTS:RP11-284F21.9 was upregulated in human OSCC samples and cell lines. RP11-284F21.9 depletion suppressed the proliferation, migration, and invasion of OSCC cell lines. There was interaction between RP11-284F21.9, miR-383-5p, and MAL2. Increased MAL2 and decreased miR-383-5p expression were also detected in OSCC tissues and cell lines. In addition, RP11-284F21.9 knockdown could reduce MAL2 expression, while miR-383-5p inhibitors abolished this repressive effect. RP11-284F21.9 acted as a competing endogenous RNA (ceRNA) of miR-383-5p, leading to MAL2 upregulation, and subsequently promoted OSCC progression. CONCLUSION:RP11-284F21.9/miR-383-5p represents a novel and potential therapeutic target for the treatment of OSCC.