Mingyan Zhu1, Jian Xie2. 1. Department of Gastroenterology, Affiliated AoYang Hospital of Jiangsu University, Zhangjiagang City, 215600, Jiangsu Province, People's Republic of China. 2. Department of Gastroenterology, The No. 1 People's Hospital of Zhangjiagang, No. 68 Jiyangxi Road, Zhangjiagang City, 215600, Jiangsu Province, People's Republic of China. rk5709@163.com.
Abstract
BACKGROUND: LncRNA MALAT1 contributes to the inflammatory responses induced by lipopolysaccharides (LPS), which shares similar pathogenesis with ulcerative colitis (UC), indicating the potential involvement of MALAT1 in UC. METHODS: Expression of MALAT1 and lncRNA ANRIL in both UC patients and healthy controls was analyzed by RT-qPCR. ROC curve analysis was used to evaluate the diagnostic value of MALAT1 for UC. Cell transfections were performed to analyze the interactions between MALAT1 and ANRIL. Cell apoptosis was analyzed by cell apoptosis assay. RESULTS: In the present study, we found that MALAT1 was upregulated in colonic mucosa tissues of UC patients in comparison with healthy controls. Plasma levels of MALAT1 were also higher in UC patients than in healthy controls, and upregulation of plasma MALAT1 distinguished UC patients from healthy controls. ANRIL was also upregulated in colonic mucosa tissues of UC patients than in that of healthy controls. ANRIL and MALAT1 were significantly and positively correlated in UC patients but not in healthy controls. Normal colonic epithelial cells with ANRIL overexpression showed no significantly changed MALAT1 overexpression, while MALAT1 overexpression led to promoted ANRIL expression. MALAT1 and ANRIL overexpression led to promoted apoptosis of FHCs. CONCLUSION: MALAT1 promotes ulcerative colitis by upregulating ANRIL.
BACKGROUND: LncRNA MALAT1 contributes to the inflammatory responses induced by lipopolysaccharides (LPS), which shares similar pathogenesis with ulcerative colitis (UC), indicating the potential involvement of MALAT1 in UC. METHODS: Expression of MALAT1 and lncRNA ANRIL in both UCpatients and healthy controls was analyzed by RT-qPCR. ROC curve analysis was used to evaluate the diagnostic value of MALAT1 for UC. Cell transfections were performed to analyze the interactions between MALAT1 and ANRIL. Cell apoptosis was analyzed by cell apoptosis assay. RESULTS: In the present study, we found that MALAT1 was upregulated in colonic mucosa tissues of UCpatients in comparison with healthy controls. Plasma levels of MALAT1 were also higher in UCpatients than in healthy controls, and upregulation of plasma MALAT1 distinguished UCpatients from healthy controls. ANRIL was also upregulated in colonic mucosa tissues of UCpatients than in that of healthy controls. ANRIL and MALAT1 were significantly and positively correlated in UCpatients but not in healthy controls. Normal colonic epithelial cells with ANRIL overexpression showed no significantly changed MALAT1 overexpression, while MALAT1 overexpression led to promoted ANRIL expression. MALAT1 and ANRIL overexpression led to promoted apoptosis of FHCs. CONCLUSION:MALAT1 promotes ulcerative colitis by upregulating ANRIL.