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J Hematol Oncol. 2019 Jan 9;12(1):3. doi: 10.1186/s13045-018-0690-5.

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

Xu M1, Chen X1,2, Lin K3, Zeng K1,2, Liu X1, Xu X1,2, Pan B1, Xu T1, Sun L4, He B1, Pan Y1, Sun H1, Wang S5.

Author information

1
General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, No. 68, Changle Road, Nanjing, 210006, China.
2
School of Medicine, Southeast University, Nanjing, 210009, China.
3
Department of Laboratory Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China.
4
Department of Laboratory Medicine, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210011, China.
5
General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, No. 68, Changle Road, Nanjing, 210006, China. sk_wang@njmu.edu.cn.

Abstract

BACKGROUND:

Abnormal 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.

METHODS:

We 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.

RESULTS:

We 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.

CONCLUSIONS:

Our study elucidated that SNHG6 acted as an oncogene in CRC, which might serve as a novel target for CRC diagnosis and therapy.

KEYWORDS:

Colorectal cancer; EZH2; SNHG6; ceRNA; microRNA

PMID:
30626446
DOI:
10.1186/s13045-018-0690-5
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