LncRNA MALAT1 Promotes Ulcerative Colitis by Upregulating lncRNA ANRIL
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ORIGINAL ARTICLE
LncRNA MALAT1 Promotes Ulcerative Colitis by Upregulating lncRNA ANRIL Mingyan Zhu1 · Jian Xie2 Received: 19 December 2019 / Accepted: 18 January 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
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. Keywords Ulcerative colitis · lncRNA MALAT1 · lncRNA ANRIL · Colonic epithelial cell · Apoptosis
Introduction Ulcerative colitis (UC) is one of the two major subtypes of inflammatory bowel diseases, which are common gastrointestinal disorders in clinical practices [1]. Without proper treatment, UC may seriously affect the life quality of patients or even cause deaths in extreme cases [1]. Although the etiology of UC is still unclear, inappropriate inflammatory response caused by foreign antigens and intestinal microbes seems to contribute to the occurrence and development of this disease [2, 3]. In recent years, incidence of UC shows an * Jian Xie [email protected] 1
Department of Gastroenterology, Affiliated AoYang Hospital of Jiangsu University, Zhangjiagang City 215600, Jiangsu Province, People’s Republic of China
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
2
increasing trend among Hispanics and Asians [4]. Therefore, a better understanding of the pathophysiological mechanisms underlay this disease is needed to facilitate clinical treatment and prevention. Although the pathogenesis of UC has not been fully elucidated, genetic factors may play central roles [5–7]. Long noncoding RNAs (lncRNAs, > 200 nt) lack protein coding ability but participate in diverse biological process
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