Long non-coding RNA SNHG5 regulates ulcerative colitis via microRNA-375 / Janus kinase-2 axis

Li, Hui; Xuan, Jianhua; Zhang, Wei; An, Zhentao; Fan, Xinyu; Lü, Min; Tian, Yaozhou

doi:10.1080/21655979.2021.1953219

Cited by 17 publications

(8 citation statements)

References 40 publications

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“…Besides the butyrate supplementation as a potential treatment for UC patients, several emerging alternatives could be effective in the treatment of UC. In the aspect of gene, the knockdown of the lncRNA (small nucleolar RNA host gene 5) SNHG5 could counteract TNF-α reduced dysfunction of intestinal epithelial cells in UC patients, which may be a promising therapy for UC [ 52 ]. Meanwhile, in the aspect of protein, increased serum glucagon-like peptide 2 (GLP-2) level, a hormone secreted by L-cells of intestinal mucosa, inducing reduced microbiota diversity and abundance, may be considered a treatment for UC patients [ 53 ].…”

Section: Discussionmentioning

confidence: 99%

Evidence for the butyrate metabolism as key pathway improving ulcerative colitis in both pediatric and adult patients

et al. 2021

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Accumulating evidence has shown many similarities and differences of gene profiles and pathways between pediatric and adult ulcerative colitis (UC) patients. In this study, we aimed to investigate the shared genes and pathways in intestinal tissues of pediatric and adult UC. Differentially expressed genes (DEGs) between pediatric and adult UC were identified via bioinformatic analysis of Gene Expression Omnibus datasets GSE87473 and GSE126124. Gene Ontology and pathway enrichment were used to analyze overlapped and distinguished DEGs. Gene Set Variation Analysis (GSVA) was utilized for contrast consistency. Mice colitis models were induced by dextran sulfate sodium (DSS) and Citrobacter rodentium. 2616 DEGs were screened out in intestinal tissues of adult UC compared with those of adult healthy controls, and 1195 DEGs in pediatrics.Same pathways between pediatric and adult UC were enriched using overlapped DEGs, mainly related to immune responses and metabolic processes, including butyrate metabolism, which was also identified by GSVA analysis. Of note, butyrate metabolism was the exclusive down-regulated pathway enriched by these two analyses, indicating that butyrate metabolism is one of the key pathways associated with both pediatric and adult UC. In addition, butyrate suppressed DSS-induced and Citrobacter rodentium-induced intestinal inflammation in mice. Therefore, the study revealed that butyrate metabolism was critical in both pediatric and adult UC. And butyrate suppressed colitis in mice, which provided a theoretical basis for the potential treatment of butyrate for UC patients.

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Section: Discussionmentioning

confidence: 99%

Evidence for the butyrate metabolism as key pathway improving ulcerative colitis in both pediatric and adult patients

et al. 2021

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“…The lactate content was detected using a lactate assay kit (Jiancheng, Nanjing, China) [ 20 ]. Briefly, cells were seeded in 96 well plates.…”

Section: Methodsmentioning

confidence: 99%

Ginsenoside Rg3 and sorafenib combination therapy relieves the hepatocellular carcinomaprogression through regulating the HK2-mediated glycolysis and PI3K/Akt signaling pathway

et al. 2022

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Hepatocellular carcinoma (HCC) is the most common pathological type of primary hepatic carcinoma. This study investigated the effects of ginsenoside Rg3 (Rg3) and sorafenib (SFN) combination therapy on HCC progression. The HCC-related data were obtained from TCGA database, and the data of HK2 mRNA, clinicopathological features, and survival outcomes were extracted using R Programming 4.0. The human hepatoma cell lines HepG2 and Bel7404 were used. Cell viability was tested using the MTT assay. Glucose consumption and lactate levels of HCC cells were detected using the corresponding kits. Western blotting was used to determine the protein expression of HK2, PI3K, and Akt. HK2 was overexpressed in patients with HCC. Compared with patients with overexpressed HK2, those with low levels of HK2 achieved a longer survival time. In addition, the Rg3 and SFN combination therapy significantly reduced cell viability, glucose consumption, lactate levels, and protein expression of HK2, PI3K, and Akt in HCC cells. Additionally, the Rg3 and SFN combination therapy exhibited a better effect than the single drug group. Inhibition of the PI3K/Akt signaling pathway or exogenous lactate intervention reversed the effects of Rg3 and SFN combination therapy in HCC cells. In conclusion, Rg3 has a synergistic effect on the sensitivity of HepG2 and Bel7404 hepatoma cells to SFN, which is related to HK2-mediated glycolysis and the PI3K/Akt signaling pathway.

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“…In cell transfection, FHC cells were transfected with circ_0001187 small interfering RNA (si-circ_0001187) or pCD5 overexpression vector, miR-1236-3p mimic or inhibitor (anti-miR-1236-3p), MYD88 siRNA (si-MYD88) or pcDNA overexpression vector, as well as negative controls (all from RibiBio, Guangzhou, China) using Lipofectamine 3000 (Invitrogen). 24 h post transfection, cells were treated with 10 ng/mL TNF-α for 12 h as previously described [ 8 ].…”

Section: Methodsmentioning

confidence: 99%

Circular RNA_0001187 participates in the regulation of ulcerative colitis development via upregulating myeloid differentiation factor 88

Ouyang

et al. 2022

Bioengineered

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Circular RNA (circRNA) had been confirmed to participate in ulcerative colitis (UC) development. Circular RNA_0001187 (Circ_0001187) had been found to be overexpressed in patients with Crohn disease. Therefore, circ_0001187 might be an important circRNA regulating intestinal inflammatory diseases. However, the role and mechanism of circ_0001187 in UC progression remains unclear. The colonic mucosal tissues were obtained from 23 UC patients and 23 healthy normal controls. Tumor necrosis factor-α (TNF-α) was used to mimic UC cell model in vitro . Cell function was assessed by cell counting kit 8 assay, EdU assay, flow cytometry, ELISA assay and oxidative stress detection. RNA interaction was confirmed by dual-luciferase reporter assay and RIP assay. Serum exosomes were isolated by ultracentrifugation and identified by transmission electron microscope. Circ_0001187 was overexpressed in UC patients. Circ_0001187 knockdown enhanced the proliferation, while suppressed apoptosis, inflammation and oxidative stress of TNF-α-induced FHC cells. Circ_0001187 acted as miR-1236-3p sponge, and the effects of circ_0001187 downregulation on TNF-α-induced FHC cell injury were overturned by miR-1236-3p inhibitor. MYD88 was targeted by miR-1236-3p, and circ_0001187 sponged miR-1236-3p to regulate MYD88. MYD88 knockdown alleviated TNF-α-induced FHC cell injury, and its upregulation revoked the inhibition effect of miR-1236-3p on TNF-α-induced FHC cell injury. High expression of circ_0001187 also was observed in the serum exosomes of UC patients. Our data confirmed that circ_0001187 facilitated UC progression through miR-1236-3p/MYD88 axis, which might be a potential treatment and diagnosis biomarker for UC.

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Long non-coding RNA SNHG5 regulates ulcerative colitis via microRNA-375 / Janus kinase-2 axis

Cited by 17 publications

References 40 publications

Evidence for the butyrate metabolism as key pathway improving ulcerative colitis in both pediatric and adult patients

Evidence for the butyrate metabolism as key pathway improving ulcerative colitis in both pediatric and adult patients

Ginsenoside Rg3 and sorafenib combination therapy relieves the hepatocellular carcinomaprogression through regulating the HK2-mediated glycolysis and PI3K/Akt signaling pathway

Circular RNA_0001187 participates in the regulation of ulcerative colitis development via upregulating myeloid differentiation factor 88

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