ArticleExperimental and therapeutic medicine2021
Overexpression of circAtp9b in ulcerative colitis is induced by lipopolysaccharides and upregulates PTEN to promote the apoptosis of colonic epithelial cells.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Crosstalk between circRNAs and the classic signaling pathways in IBD.RNA biology · 2026Review
- Review
- Circular RNAs in inflammatory bowel disease: a review of mechanisms, biomarkers and therapeutic potential.Frontiers in immunology · 2025Review
- Protective role of circRNA CCND1 in ulcerative colitis via miR-142-5p/NCOA3 axis.BMC gastroenterology · 2023Article
- Circular RNAs in inflammatory bowel disease.Frontiers in immunology · 2023Review
- Circular RNA_0001187 participates in the regulation of ulcerative colitis development via upregulating myeloid differentiation factor 88.Bioengineered · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been reported that knockdown of circular RNA (circ) ATPase class II type 9B (Atp9b) can reduce lipopolysaccharide (LPS)-induced inflammation, which plays a notable role in ulcerative colitis (UC). The present study aimed to explore the role of circAtp9b in UC. The expression levels of Atp9b and PTEN in the plasma of patients with UC (n=60) and healthy controls (n=60) were determined via reverse transcription-quantitative PCR. Overexpression of circAtp9b and PTEN were achieved in human colonic epithelial cells (HCnEpCs) to explore the relationship between circAtp9b and PTEN. The role of circAtp9b and PTEN in regulating the apoptosis of HCnEpCs under LPS treatment was evaluated using flow cytometry. The present study revealed that circAtp9b was upregulated in UC and that it was positively correlated with PTEN. In HCnEpCs, LPS treatment resulted in upregulation of circAtp9b in a dose-dependent manner. Moreover, overexpression of circAtp9b mediated the upregulation of PTEN in HCnEpCs, while silencing of circAtp9b decreased the expression levels of PTEN. Apoptosis analysis demonstrated that overexpression of circAtp9b and PTEN promoted the apoptosis of HCnEpCs. In addition, silencing of circAtp9b suppressed apoptosis. Moreover, overexpression of PTEN reduced the effects of silencing of circAtp9b. In conclusion, overexpression of circAtp9b in UC was induced by LPS and it positively upregulated PTEN to promote the apoptosis of HCnEpCs induced by LPS.
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Registered trials
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