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LncRNA SNHG6 is Associated with Poor Prognosis of Gastric Cancer and Promotes Cell Proliferation and EMT through Epigenetically Silencing p27 and Sponging miR-101-3p
- Source :
- Cellular Physiology and Biochemistry, Vol 42, Iss 3, Pp 999-1012 (2017)
- Publication Year :
- 2017
- Publisher :
- Cell Physiol Biochem Press GmbH & Co KG, 2017.
-
Abstract
- Background/Amis: Long non-coding RNAs (lncRNAs), a novel class of transcripts, have been shown to play critical roles in diverse cellular biological processes, including tumorigenesis. Small nucleolar RNA host gene 6 (SNHG6) regulates various biological processes in cancer cells. However, the biological role of SNHG6 in gastric cancer still remains to be explored. The aim of this study is to investigate the characteristic of the SNHG6 in gastric cancer. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the expression of SNHG6 in gastric cancer tissues and cell lines. MTT assays, colony formation assays were used to determine the impact of SNHG6 on tumorigenesis . Flow cytometric analysis of cell cycle and apoptosis was performed to measure the effect of SNHG6 on cell cycle and apoptosis rate. Transwell assay was performed to measure the effect of SNHG6 on cell migration. Western blotting and immunofuorescence were utilized to examine the effect of SNHG6 on epithelial-mesenchymal transition (EMT) of GC cells. Chromatin immunoprecipitation (ChIP), RNA immunoprecipitation (RIP), RNA-pulldown and luciferase reporter assays were employed to dissect molecular mechanisms. Results: In this study, we revealed that SNHG6 was overexpressed in gastric cancer tissues and cell lines. High expression levels of SNHG6 wereassociated with invasion depth, lymph node metastasis, distant metastasis and tumor/node/metastasis (TNM) stage, and predicted poor prognosis. Loss-of-function assays revealed that silenced SNHG6 obviously inhibited gastric cancer cell growth, weakened cell migration capacity and suppressed the EMT processes of gastric cancer cells. Additionally, ChIP, RIP, RNA-pulldown and luciferase reporter assays evidenced that SNHG6 could epigenetically silenced p27 and could competitively sponging miR-101-3p thereby regulating zinc finger E-box-binding homeobox 1 (ZEB1). Conclusion: In summary, our findings demonstrated that SNHG6 acted as an oncogene in gastric cancer cells through regulating miR-101-3p/ZEB1 at a post-transcriptional level and silencing expression at a transcriptional level by recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p27. SNHG6 might serve as a candidate prognostic biomarker and a target for novel therapies of gastric cancer patients.
- Subjects :
- Male
0301 basic medicine
Poor prognosis
Epithelial-Mesenchymal Transition
Physiology
Apoptosis
Biology
Bioinformatics
lcsh:Physiology
Epigenesis, Genetic
lcsh:Biochemistry
03 medical and health sciences
0302 clinical medicine
Cell Movement
Stomach Neoplasms
Cell Line, Tumor
medicine
SNHG6
Humans
Gene silencing
ZEB1
Neoplasm Invasiveness
lcsh:QD415-436
EZH2
miR-101-3p
Cell Proliferation
lcsh:QP1-981
Cell growth
Stomach
EMT
Cancer
Mir 101 3p
p27
Cell Cycle Checkpoints
Middle Aged
Prognosis
medicine.disease
Up-Regulation
Gene Expression Regulation, Neoplastic
MicroRNAs
030104 developmental biology
030220 oncology & carcinogenesis
Female
RNA, Long Noncoding
Gastric cancer
Cyclin-Dependent Kinase Inhibitor p27
Subjects
Details
- Language :
- English
- ISSN :
- 14219778 and 10158987
- Volume :
- 42
- Issue :
- 3
- Database :
- OpenAIRE
- Journal :
- Cellular Physiology and Biochemistry
- Accession number :
- edsair.doi.dedup.....beae8849535b6d8bfa75c144afacf983