Lin Fang1, Mengcheng Hu1, Fei Xia1, Wenxia Bai1. 1. Department of Gastroenterology, The Affiliated Jiangning Hospital of Nanjing Medical University Nanjing 211100, Jangsu, China.
Abstract
OBJECTIVES: Long noncoding RNAs (lncRNAs) have different functions in different diseases. There is little research on the functions of lncRNAs in Crohn's disease (CD). By using RNA-seq technology, we identified a lncRNA associated with Crohn's disease. However, the mechanism of lncRNA regulation remains unknown. This study aimed to determine the association of LINC01272 with epithelial cell-mesenchymal transition and the underlying mechanism in CD. METHODS: RNA was detected by qRT-PCR. The interaction of protein and RNA was determined by RNA binding protein immunoprecipitation. Luciferase reporter assays were used to detect the targeted miRNA of LINC01272. Tissue fibrosis was observed by Masson and H&E staining. Protein expression was determined by western blotting and immunofluorescence. RESULTS: LINC01272 was highly expressed in patients with CD. Knockdown of LINC01272 inhibited TGF-β1-induced epithelial-mesenchymal transition (EMT). Additionally, LINC01272 regulated TGF-β1-induced EMT through the miR-153-5p axis, and knockdown of LINC01272 inhibited EMT in CD mice in vivo. CONCLUSION: LINC01272 activated the epithelial-mesenchymal transition through miR-153-5p in CD. AJTR
OBJECTIVES: Long noncoding RNAs (lncRNAs) have different functions in different diseases. There is little research on the functions of lncRNAs in Crohn's disease (CD). By using RNA-seq technology, we identified a lncRNA associated with Crohn's disease. However, the mechanism of lncRNA regulation remains unknown. This study aimed to determine the association of LINC01272 with epithelial cell-mesenchymal transition and the underlying mechanism in CD. METHODS: RNA was detected by qRT-PCR. The interaction of protein and RNA was determined by RNA binding protein immunoprecipitation. Luciferase reporter assays were used to detect the targeted miRNA of LINC01272. Tissue fibrosis was observed by Masson and H&E staining. Protein expression was determined by western blotting and immunofluorescence. RESULTS: LINC01272 was highly expressed in patients with CD. Knockdown of LINC01272 inhibited TGF-β1-induced epithelial-mesenchymal transition (EMT). Additionally, LINC01272 regulated TGF-β1-induced EMT through the miR-153-5p axis, and knockdown of LINC01272 inhibited EMT in CD mice in vivo. CONCLUSION: LINC01272 activated the epithelial-mesenchymal transition through miR-153-5p in CD. AJTR
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