lncRNA SNHG6 regulates EZH2 expression by sponging miR-26a/b and miR-214 in colorectal cancer

被引:180
作者
Xu, Mu [1 ]
Chen, Xiaoxiang [1 ,2 ]
Lin, Kang [3 ]
Zeng, Kaixuan [1 ,2 ]
Liu, Xiangxiang [1 ]
Xu, Xueni [1 ,2 ]
Pan, Bei [1 ]
Xu, Tao [1 ]
Sun, Li [4 ]
He, Bangshun [1 ]
Pan, Yuqin [1 ]
Sun, Huiling [1 ]
Wang, Shukui [1 ]
机构
[1] Nanjing Med Univ, Nanjing Hosp 1, Gen Clin Res Ctr, 68 Changle Rd, Nanjing 210006, Jiangsu, Peoples R China
[2] Southeast Univ, Sch Med, Nanjing 210009, Jiangsu, Peoples R China
[3] Nanjing Med Univ, Nanjing Hosp 1, Dept Lab Med, Nanjing 210006, Jiangsu, Peoples R China
[4] Nanjing Med Univ, Dept Lab Med, Affiliated Hosp 2, Nanjing 210011, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
SNHG6; EZH2; microRNA; Colorectal cancer; ceRNA; LONG NONCODING RNA; CELL-PROLIFERATION; TRANSCRIPTION; PROGRESSION; BINDING; CLASSIFICATION; METASTASIS; POLYCOMB; DATABASE; PROTEIN;
D O I
10.1186/s13045-018-0690-5
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
BackgroundAbnormal expression of long non-coding RNAs (lncRNAs) has been found in almost all human tumors, providing numerous potential diagnostic biomarkers, prognostic biomarkers, and therapeutic targets.MethodsWe analyzed RNA sequencing data to explore abnormally expressed lncRNAs in colorectal cancer (CRC). The functions of small nucleolar RNA host gene 6 (SNHG6) were investigated through in vitro and in vivo assays (CCK-8 assay, colony formation assay, flow cytometry assay, EdU assay, wound healing assay, transwell assay, and xenograft model). The mechanism of action of SNHG6 was explored through bioinformatics, RNA fluorescence in situ hybridization, luciferase reporter assay, RNA pull-down assay, chromatin immunoprecipitation assay, and RNA immunoprecipitation assay.ResultsWe identified aberrantly expressed lncRNAs in CRC. We found that elevated SNHG6 expression was associated with poor prognosis and CRC progression. We also demonstrated that the high SNHG6 expression was partly due to DNA copy number gains and SP1 induction. Functional studies showed that SNHG6 promoted CRC cell growth, migration, and invasion both in vitro and in vivo. Mechanistically, we found that SNHG6 expressed predominantly in the cytoplasm. SNHG6 could interact with miR-26a, miR-26b, and miR-214 and regulate their common target EZH2.ConclusionsOur study elucidated that SNHG6 acted as an oncogene in CRC, which might serve as a novel target for CRC diagnosis and therapy.
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页数:17
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