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LncRNA MALAT1 Promotes Ulcerative Colitis by Upregulating lncRNA ANRIL

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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.

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Authors and Affiliations

  1. Department of Gastroenterology, Affiliated AoYang Hospital of Jiangsu University, Zhangjiagang City, 215600, Jiangsu Province, People’s Republic of China

    Mingyan Zhu

  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

    Jian Xie

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  1. Mingyan Zhu
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  2. Jian Xie
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Correspondence to Jian Xie.

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Zhu, M., Xie, J. LncRNA MALAT1 Promotes Ulcerative Colitis by Upregulating lncRNA ANRIL. Dig Dis Sci 65, 3191–3196 (2020). https://doi.org/10.1007/s10620-020-06093-w

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  • DOI: https://doi.org/10.1007/s10620-020-06093-w

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