4.6 Article

Long noncoding ribonucleic acid specific for distant metastasis of gastric cancer is associated with TRIM16 expression and facilitates tumor cell invasion in vitro

期刊

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
卷 30, 期 9, 页码 1367-1375

出版社

WILEY
DOI: 10.1111/jgh.12976

关键词

gastric cancer; invasion; LOC100507069; long noncoding RNA; metastasis

资金

  1. National Natural Science Foundation of China [81372290, 81372291]
  2. Specialized Research Fund for the Doctoral Program of Higher Education [20130001120064]
  3. Peking University People's Hospital Research and Development Funds of China [RDB2012-19, RDB 2013-15]

向作者/读者索取更多资源

Background and AimIncreasing 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. MethodsDifferentially 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. Results502 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. ConclusionsSDMGC is obviously upregulated in stage IV GC and may represent a new marker and therapeutic target for GC treatment.

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