ArticleEuropean journal of gastroenterology & hepatology2021
Long noncoding RNA KIF9-AS1 promotes cell apoptosis by targeting the microRNA-148a-3p/suppressor of cytokine signaling axis in inflammatory bowel disease.
Article in European journal of gastroenterology & hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- ceRNA Network Dynamics in Inflammatory Bowel Disease: The LncRNA-miRNA-mRNA Axis in Intestinal Homeostasis and Inflammation.Cell biochemistry and biophysics · 2026Review
- UHRF1 deficiency exacerbates intestinal inflammation by epigenetic modulation of NPY1R gene methylation.JCI insight · 2026Article
- Article
- Milk-Derived Extracellular Vesicles and microRNAs: Potential Modulators of Intestinal Homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Value of serum LncRNA KIF9-AS1 combined with CT signs in the diagnosis of benign and malignant early pulmonary nodules and its correlation with prognosis.Journal of cardiothoracic surgery · 2025Article
- Mechanism underlying the role of the circRNA OMA1/miR-654-3p/RAF1 axis in children with inflammatory bowel disease.Cytotechnology · 2025Article
- Expression and role of CTHRC1 in inflammatory bowel disease in children.Cytotechnology · 2025Article
- The significance of long non-coding RNAs in the pathogenesis, diagnosis and treatment of inflammatory bowel disease.Precision clinical medicine · 2023Review
- The Role of Long Noncoding RNAs in Intestinal Health and Diseases: A Focus on the Intestinal Barrier.Biomolecules · 2023Review
- Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveInflammatory bowel disease (IBD) is a chronic intestinal disease. This study was attempted to investigate the effects of long noncoding RNA KIF9-AS1 (KIF9-AS1) on the development of IBD and its underlying mechanism of action.
methodsQuantitative real time PCR (qRT-PCR) was implemented to examine the expression of KIF9-AS1 and microRNA-148a-3p (miR-148a-3p). The IBD mouse model was induced by dextran sulfate sodium (DSS). The body weight, disease activity index (DAI) score, colon length and histological injury were used to evaluate the colon injury. The levels of proinflammatory cytokines were measured by ELISA. In vitro, IBD was simulated by DSS treatment in colonic cells. Then the apoptosis of colonic cells was detected by flow cytometry assay. Furthermore, a dual-luciferase reporter assay was used to demonstrate the interactions among KIF9-AS1, miR-148a-3p and suppressor of cytokine signaling (SOCS3).
resultsKIF9-AS1 expression was upregulated in IBD patients, DSS-induced IBD mice and DSS-induced colonic cells, whereas miR-148a-3p expression was downregulated. KIF9-AS1 silencing attenuated the apoptosis of DSS-induced colonic cells in vitro and alleviated colon injury and inflammation in DSS-induced IBD mice in vivo. Additionally, the mechanical experiment confirmed that KIF9-AS1 and SOCS3 were both targeted by miR-148a-3p with the complementary binding sites at 3'UTR. Moreover, miR-148a-3p inhibition or SOCS3 overexpression reversed the suppressive effect of KIF9-AS1 silencing on the apoptosis of DSS-induced colonic cells.
conclusionKIF9-AS1 silencing hampered the colon injury and inflammation in DSS-induced IBD mice in vivo, and restrained the apoptosis of DSS-induced colonic cells by regulating the miR-148a-3p/SOCS3 axis in vitro, providing a new therapeutic target for IBD.
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