【摘 要】
：
Gastric cancer(GC)is thought to be driven by long noncoding RNA(lncRNA),lipid metabolism and the activation of the oncogene,but it is uncertain how they may become coordinated during the gastric carci
【机 构】
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Department of Biochemistry,School of Preclinical Medicine,North Sichuan Medical College,Nanchong,Sic
【出 处】
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中国生物化学与分子生物学会2016年全国学术会议
论文部分内容阅读
Gastric cancer(GC)is thought to be driven by long noncoding RNA(lncRNA),lipid metabolism and the activation of the oncogene,but it is uncertain how they may become coordinated during the gastric carcinogenesis.The present study reports that the lncRNA LINC00152 acts as a competing endogenous RNA(ceRNA)to regulate the expression of fatty acid synthase(FASN)by taking up miR-497 in gastric cancer.Our results show that LINC00152 was upregulated in gastric cancer cells and that its abundance corresponded with that of FASN mRNA.Both of them were negatively regulated by miR-497.Further experiments demonstrated that LINC00152 upregulation inhibits miR-497 and elevates the levels of FASN mRNA and protein.Moreover,LINC00152 upregulation accelerates cell proliferation and synthesis of fatty acid.Overall,our results offer a strong mechanistic rationale to lncRNAs function in tumorigenesis that lncRNAs acts as ceRNAs for tumor promoters mRNAs.
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