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Long noncoding ribonucleic acid specific for distant metastasis of gastric cancer is associated with TRIM 16 expression and facilitates tumor cell invasion in vitro
Author(s) -
Yan Yichao,
Shen Zhanlong,
Gao Zhidong,
Cao Jian,
Yang Yang,
Wang Bo,
Shen Chao,
Mao Shuqiang,
Jiang Kewei,
Ye Yingjiang,
Wang Shan
Publication year - 2015
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.12976
Subject(s) - gene silencing , long non coding rna , metastasis , biology , rna interference , cancer research , cancer , downregulation and upregulation , gene , gene expression , cell cycle , microrna , microarray , cell growth , cell , rna , genetics
Abstract Background and Aim Increasing evidence has indicated that long noncoding ribonucleic acids ( lncRNAs ) play a major role in cancers. Although certain lncRNAs has been reported to play a role in gastric cancer ( GC ), specific lncRNAs involved in distant metastasis of GC remain unknown. Methods Differentially expressed mRNAs and lncRNAs between stage IV and non‐stage IV GC were obtained by microarray. Gene ontology and pathway analysis were used to study functions of differential mRNAs . Algorithms were used to predict potential gene targets of cis or trans ‐acting lncRNAs . Network analysis was performed to analyze each pair of gene– lncRNA , gene–gene, or lncRNA–lncRNA interactions. Expression of lncRNA special for distant metastasis of GC ( SDMGC ) and target gene TRIM16 were tested in GC tissues and cell lines. RNAi and overexpression were used to observe the biological functions of SDMGC and TRIM16 on GC cells. Results 502 mRNAs and 440 lncRNAs were found to be differentially expressed. 74 gene ontology terms and 38 pathways were associated with the dysregulated transcripts. Fourteen core factors were determined by network analysis. Expression of SDMGC and TRIM16 was upregulated in the distant metastasis tissues, compared with primary GC tissues, which were positive correlation. Silencing of SDMGC or TRIM16 was demonstrated to decrease cell invasion and migration, while upregulated of SDMGC or TRIM16 could promote cell invasion and migration. However, little effect on proliferation, cell cycle, colony formation, and apoptosis was found. Conclusions SDMGC is obviously upregulated in stage IV GC and may represent a new marker and therapeutic target for GC treatment.