Overexpression of circAtp9b in ulcerative colitis is induced by lipopolysaccharides and upregulates PTEN to promote the apoptosis of colonic epithelial cells

Li, Fengdong; Fu, Jinjin; Фан, Ли; Lu, Shuangshuang; Zhang, Huahui; Wang, Xiaoying; Liu, Zhanju

doi:10.3892/etm.2021.10840

Cited by 7 publications

(6 citation statements)

References 22 publications

(24 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…27 In addition, circAtp9b, which was overexpressed in UC patients, had been shown to promote LPS-induced colonic epithelial cell apoptosis. 28 These results confirm the importance of circRNA in regulating UC process. Although previous studies have shown that circSOD2 may contribute to UC development by weakening the intestinal barrier, 13 more evidence is needed to further support the conclusion that circSOD2 is a potential target for treating UC.…”

Section: Discussionsupporting

confidence: 66%

CircSOD2: Disruption of intestinal mucosal barrier function in ulcerative colitis by regulating the miR‐378g/Snail1 axis

Ye,

Zhang,

Peng

et al. 2024

J of Gastro and Hepatol

View full text Add to dashboard Cite

Background and AimCircular RNA (circRNA) has been found to mediate ulcerative colitis (UC) progression by regulating intestinal mucosal barrier function. However, the role of circSOD2 in UC process and its underlying molecular mechanism still need to be further elucidated.MethodsLipopolysaccharide (LPS)‐induced Caco2 cells were used to mimic UC cell models. CircSOD2, miR‐378g, and Snail1 levels were determined by quantitative real‐time PCR. Cell viability was detected using MTT assay, and inflammatory cytokine levels were measured using ELISA. The intestinal mucosal barrier function was evaluated by testing transepithelial electrical resistance and fluorescein isothiocyanate (FITC)‐dextran permeability. Snail1 and tight junction‐related markers (Zo‐1 and Claudin2) protein levels were examined using western blot. The interaction between miR‐378g and circSOD2 or Snail1 was confirmed by dual‐luciferase reporter assay. Dextran sulfate sodium (DSS) was used to induce UC rat models in vivo.ResultsCircSOD2 was overexpressed in UC patients, and its knockdown significantly increased cell viability, transepithelial electrical resistance, and tight junction‐related protein expression, while reduced inflammation cytokine levels and the permeability of FITC‐dextran in LPS‐induced Caco2 cells. In terms of mechanism, circSOD2 sponged miR‐378g to positively regulate Snail1 expression. MiR‐378g inhibitor reversed the effect of circSOD2 knockdown on intestinal mucosal barrier injury and Snail1 expression in LPS‐induced Caco2 cells. In DSS‐induced UC rat models, circSOD2 knockdown also could repair the intestinal mucosal barrier injury through regulating miR‐378g/Snail1 axis.ConclusionCircSOD2 could destroy intestinal mucosal barrier function in LPS‐induced Caco2 cells and DSS‐induced UC rats by miR‐378g/Snail1 axis.

show abstract

Section: Discussionsupporting

confidence: 66%

CircSOD2: Disruption of intestinal mucosal barrier function in ulcerative colitis by regulating the miR‐378g/Snail1 axis

Ye,

Zhang,

Peng

et al. 2024

J of Gastro and Hepatol

View full text Add to dashboard Cite

show abstract

“…Upregulated expression of circAtp9b was observed in plasma samples from UC patients ( 112 ). LPS treatment increased the expression of circAtp9b in human colonic epithelial cells, which increased the expression of PTEN, eventually promoting apoptosis in colonic epithelial cells.…”

Section: Roles Of Circrnas In Ibdmentioning

confidence: 99%

Circular RNAs in inflammatory bowel disease

Lun,

Guo,

et al. 2023

Front. Immunol.

View full text Add to dashboard Cite

Inflammatory bowel disease (IBD) is a term encompassing a few chronic inflammatory disorders that leads to damage of the intestinal tract. Although much progress has been made in understanding the pathology of IBD, the precise pathogenesis is not completely understood. Circular RNAs (circRNAs) are single-stranded, covalently closed, endogenous molecules in eukaryotes with a variety of biological functions. CircRNAs have been shown to have regulatory effects in many diseases, such as cancer, cardiovascular disease, and neurological disorders. CircRNAs have also been found to play important roles in IBD, and although they are not sufficiently investigated in the context of IBD, a few circRNAs have been identified as potential biomarkers for the diagnosis and prognosis of IBD and as potential therapeutic targets for IBD. Herein, we survey recent progress in understanding the functions and roles of circRNAs in IBD and discuss their potential clinical applications.

show abstract

“…IL-3 is involved in UC through circular RNA circPan3 [ 10 ]. In ulcerative colitis, circRNA Atp9b is overexpressed [ 11 ]. CircRNA CCND1 is a new circRNA that has been shown to expedite cell metastasis and proliferation in hepatocellular carcinoma tumorigenesis by regulating the miR-497-5p/HMGA2 axis [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Protective role of circRNA CCND1 in ulcerative colitis via miR-142-5p/NCOA3 axis

Xiang

Zhou

et al. 2023

BMC Gastroenterol

View full text Add to dashboard Cite

Background Increasing research indicates that circular RNAs (circRNAs) play critical roles in the development of ulcerative colitis (UC). This study aimed to determine the role of circRNA CCND1 in UC bio-progression, which has been shown to be downregulated in UC tissues. Methods Reverse transcription quantitative polymerase chain reaction was used to determine the levels of circRNA CCND1, miR-142-5p, and nuclear receptor coactivator-3 (NCOA3) in UC tissues and in lipopolysaccharide (LPS)-induced Caco-2 cells. Target sites of circRNA CCND1 and miR-142-5p were predicted using StarBase, and TargetScan to forecast potential linkage points of NCOA3 and miR-142-5p, which were confirmed by a double luciferase reporter-gene assay. Cell Counting Kit 8 and flow cytometry assays were performed to assess Caco-2 cell viability and apoptosis. TNF-α, IL-1β, IL-6, and IL-8 were detected using Enzyme-Linked Immunosorbent Assay kits. Results CircRNA CCND1 was downregulated in UC clinical samples and LPS-induced Caco-2 cells. In addition, circRNA CCND1 overexpression suppressed LPS-induced apoptosis and inflammatory responses in Caco-2 cells. Dual-luciferase reporter-gene assays showed that miR-142-5p could be linked to circRNA CCND1. Moreover, miR-142-5p was found to be highly expressed in UC, and its silencing inhibited LPS-stimulated Caco-2 cell apoptosis and inflammatory responses. Importantly, NCOA3 was found downstream of miR-142-5p. Overexpression of miR-142-5p reversed the inhibitory effect of circRNA CCND1-plasmid on LPS-stimulated Caco-2 cells, and the effects of miR-142-5p inhibitor were reversed by si-NCOA3. Conclusion CircRNA CCND1 is involved in UC development by dampening miR-142-5p function, and may represent a novel approach for treating UC patients.

show abstract

Overexpression of circAtp9b in ulcerative colitis is induced by lipopolysaccharides and upregulates PTEN to promote the apoptosis of colonic epithelial cells

Cited by 7 publications

References 22 publications

CircSOD2: Disruption of intestinal mucosal barrier function in ulcerative colitis by regulating the miR‐378g/Snail1 axis

CircSOD2: Disruption of intestinal mucosal barrier function in ulcerative colitis by regulating the miR‐378g/Snail1 axis

Circular RNAs in inflammatory bowel disease

Protective role of circRNA CCND1 in ulcerative colitis via miR-142-5p/NCOA3 axis

Contact Info

Product

Resources

About