Which long noncoding RNAs and circular RNAs contribute to inflammatory bowel disease?

Lin, Lihui; Zhou, Gaoshi; Chen, Peng; Wang, Ying; Han, Jing; Chen, Minhu; He, Yao; Zhang, Shenghong

doi:10.1038/s41419-020-2657-z

Cited by 48 publications

(37 citation statements)

References 145 publications

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“…GPR25 is a G protein-coupled receptor that is highly expressed in T cells and NK cells and has been shown to be involved in the risk of MS and IBD 60 . In contrast, little is known about the function of lncRNAs AL133458.1, or of antisense gene LL22NC03-86G7.1 or pseudogene AC100854.1, but pseudogenes and non-coding RNAs have previously been hypothesised to make crucial contributions to comorbid MS 61,62 and IBD 63,64 .…”

Section: Discussionmentioning

confidence: 99%

Investigating the shared genetic architecture between multiple sclerosis and inflammatory bowel diseases

et al. 2021

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An epidemiological association between multiple sclerosis (MS) and inflammatory bowel disease (IBD) is well established, but whether this reflects a shared genetic aetiology, and whether consistent genetic relationships exist between MS and the two predominant IBD subtypes, ulcerative colitis (UC) and Crohn’s disease (CD), remains unclear. Here, we use large-scale genome-wide association study summary data to investigate the shared genetic architecture between MS and IBD overall and UC and CD independently. We find a significantly greater genetic correlation between MS and UC than between MS and CD, and identify three SNPs shared between MS and IBD (rs13428812), UC (rs116555563) and CD (rs13428812, rs9977672) in cross-trait meta-analyses. We find suggestive evidence for a causal effect of MS on UC and IBD using Mendelian randomization, but no or weak and inconsistent evidence for a causal effect of IBD or UC on MS. We observe largely consistent patterns of tissue-specific heritability enrichment for MS and IBDs in lung, spleen, whole blood and small intestine, and identify cell-type-specific enrichment for MS and IBDs in CD4+ T cells in lung and CD8+ cytotoxic T cells in lung and spleen. Our study sheds light on the biological basis of comorbidity between MS and IBD.

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Section: Discussionmentioning

confidence: 99%

Investigating the shared genetic architecture between multiple sclerosis and inflammatory bowel diseases

et al. 2021

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“…CircRNAs are considered important regulatory molecules in large numbers of biological processes involved in various diseases (Lin et al, 2020). An increasing number of studies have reported that circRNAs play important roles in the pathogenesis of IBD.…”

Section: Discussionmentioning

confidence: 99%

Hsa_circRNA_103124 Upregulation in Crohn’s Disease Promotes Cell Proliferation and Inhibits Autophagy by Regulating the Hsa-miR-650/AKT2 Signaling Pathway

Yin

Tong

et al. 2021

Front. Genet.

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Circular RNAs (circRNAs) play important roles in the pathogenesis of Crohn’s disease (CD). We discovered that hsa_circRNA_103124 was upregulated in CD patients in our previous study. Nonetheless, the function of hsa_circRNA_103124 is unclear. In this study, hsa_circRNA_103124 was predicted to interact with hsa-miR-650. Gene Ontology (GO) and pathway analyses identified AKT serine/threonine kinase 2 (AKT2) as the downstream target protein of hsa-miR-650. Activated AKT2 inhibits autophagy, but promotes cell proliferation. Recent studies suggest that the inhibition of autophagy is one of the mechanisms of CD pathogenesis. Therefore, we inferred that hsa_circRNA_103124 might regulate autophagy and proliferation by targeting AKT2 as a sponge for hsa-miR-650. Here, quantitative reverse transcription PCR (RT-QPCR) results revealed that upregulated hsa_circRNA_103124 expression in patients with CD was negatively correlated with hsa-miR-650 expression but positively correlated with the white blood cell count and calprotectin levels. TSC complex subunit 1 (TSC1), one of the proteins upstream of autophagy was downregulated in patients with CD. Consisting with the bioinformatics prediction, it was verified that hsa_circRNA_103124 targeted to hsa-miR650 by fluorescence in situ hybridization (FISH) and luciferase reporter assays. A hsa-miR-650 inhibitor reversed the promotion of rapamycin-induced autophagy and the inhibition of cell proliferation by the hsa_circRNA_103124 siRNA. However, hsa-miR-650 mimics reversed the inhibition of rapamycin-induced autophagy and the promotion of cell proliferation through hsa_circRNA_103124 overexpression. These results indicate that hsa_circRNA_103124 upregulation in patients with CD promotes cell proliferation and inhibits autophagy by regulating the hsa-miR-650/AKT2 signaling pathway.

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“…Meanwhile, correlations between circRIMS1 and clinical or pathological stages and histological grades will also be investigated. circRNAs have been reported to participate in the initiation and progression of sepsis, 43 schizophrenia, depression, 44 inflammatory bowel disease, 45 autoimmune diseases, 46 and especially human cancers. 47 , 48 , 49 , 50 , 51 , 52 Therefore, it is reasonable to speculate that they are also potential therapeutic targets.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA circRIMS1 Acts as a Sponge of miR-433-3p to Promote Bladder Cancer Progression by Regulating CCAR1 Expression

Wang

Fan

Cai

et al. 2020

Molecular Therapy - Nucleic Acids

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Circular RNAs (circRNAs), a subclass of noncoding RNAs, are reportedly involved in the progression of various diseases. However, the exact role of circRIMS1, also termed hsa_circ_0132246, in human bladder cancer remains unknown. By performing RNA sequencing comparing bladder cell lines and normal uroepithelial cells, circRIMS1 was selected as a research object. We further verified by qRT-PCR that circRIMS1 is upregulated in both bladder cancer tissue and cell lines. Proliferation, colony-formation, Transwell migration, invasion, apoptosis, western blotting, and in vivo experiments were utilized to clarify the roles of circRIMS1, microRNA (miR)-433-3p, and cell cycle and apoptosis regulator 1 (CCAR1). For mechanistic investigation, RNA pulldown, fluorescence in situ hybridization (FISH), and luciferase reporter assay confirmed the binding of circRIMS1 with miR-433-3p. Inhibition of circRIMS1 suppressed the proliferation, migration, and invasion of bladder cancer cells both in vitro and in vivo . Moreover, the circRIMS1/miR-433-3p/CCAR1 regulatory axis was confirmed to be responsible for the biological functions of circRIMS1. Taken together, our research demonstrated that circRIMS1 promotes tumor growth, migration, and invasion through the miR-433-3p/CCAR1 regulatory axis, representing a potential therapeutic target and biomarker in bladder cancer.

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Which long noncoding RNAs and circular RNAs contribute to inflammatory bowel disease?

Cited by 48 publications

References 145 publications

Investigating the shared genetic architecture between multiple sclerosis and inflammatory bowel diseases

Investigating the shared genetic architecture between multiple sclerosis and inflammatory bowel diseases

Hsa_circRNA_103124 Upregulation in Crohn’s Disease Promotes Cell Proliferation and Inhibits Autophagy by Regulating the Hsa-miR-650/AKT2 Signaling Pathway

Circular RNA circRIMS1 Acts as a Sponge of miR-433-3p to Promote Bladder Cancer Progression by Regulating CCAR1 Expression

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