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RP11‐284F21.9 promotes oral squamous cell carcinoma development via the miR‐383‐5p/MAL2 axis
Author(s) -
Shao Bingyi,
Fu Xiaohui,
Li Xian,
Li Yong,
Gan Ning
Publication year - 2020
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12946
Subject(s) - gene knockdown , downregulation and upregulation , competing endogenous rna , cancer research , carcinogenesis , cell growth , biology , microrna , cell culture , cell , transfection , rna , cell migration , cancer , long non coding rna , microbiology and biotechnology , gene , genetics
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.