Lipopolysaccharide-induced lung cell inflammation and apoptosis are enhanced by circ_0003420/miR-424-5p/TLR4 axis via inactivating the NF-κB signaling pathway
“…10 Further study revealed that polysaccharides of Dangshen could effectively inhibit the proliferation of gastric cancer AGS cells, induce apoptosis and inhibit the secretion of pro-inflammatory factors, the mechanism of which may be related to the regulation of the miR-361-5p/ TLR4/NF-κB pathway. 11 Based on the above study, we propose the hypothesis that DHJ may have a protective effect on the gastric mucosa.…”
One of the top ten tonic herbs, dangshen is frequently found in Chinese functional foods. With the inclusion of dangshen in the list of food and medicine substances in 2020,...
“…10 Further study revealed that polysaccharides of Dangshen could effectively inhibit the proliferation of gastric cancer AGS cells, induce apoptosis and inhibit the secretion of pro-inflammatory factors, the mechanism of which may be related to the regulation of the miR-361-5p/ TLR4/NF-κB pathway. 11 Based on the above study, we propose the hypothesis that DHJ may have a protective effect on the gastric mucosa.…”
One of the top ten tonic herbs, dangshen is frequently found in Chinese functional foods. With the inclusion of dangshen in the list of food and medicine substances in 2020,...
“…In mechanism, miR-424-5p was predicted to bind with circRNA_0001006 and was reported to serve as a tumor suppressor in breast cancer. miR-424-5p was also involved in the function of many other circRNAs, such as the inhibition of gastric cancer cells by circ_LARP4, the promoter role of circ_RNF13 in HBV-hepatocellular carcinoma, and the enhancement of lung cell inflammation by cicr_0003420 [ 11 – 13 ]. Therefore, circRNA_0001006 might regulate the development of TNBC, and whether miR-424-5p mediates the function of circ_0001006 was also estimated.…”
Background
circular RNAs (circRNAs) have been considered novel biomarker candidates for human cancers, such as triple-negative breast cancer (TNBC). circ_0001006 was identified as a differentially expressed circRNA in metastatic breast cancer, but its significance and function in TNBC were unclear. The significance of circ_0001006 in TNBC was assessed and exploring its potential molecular mechanism to provide a therapeutic target for TNBC.
Results
circ_0001006 showed significant upregulation in TNBC and close association with patients’ histological grade, Ki67 level, and TNM stage. Upregulated circ_0001006 could predict a worse prognosis and high risk of TNBC patients. In TNBC cells, silencing circ_0001006 suppressed cell proliferation, migration, and invasion. In mechanism, circ_0001006 could negatively regulate miR-424-5p, which mediated the inhibition of cellular processes by circ_0001006 knockdown.
Conclusions
Upregulated circ_0001006 in TNBC served as a poor prognosis predictor and tumor promoter via negatively regulating miR-424-5p.
“…Shen et al (14) underscored that circ_0003091 was involved in lung injury, apoptosis, and inflammation in a SA-ALI mouse model by targeting miR-149/Smad2 pathway. Yang et al (15) demonstrated circ_0003420 deficiency alleviated LPS-mediated lung injury and inflammatory processes by targeting miR-424-5p and regulating TLR4 levels. Zhu et al (16) uncovered that circ_0001679 was elevated in LPS-stimulated MLE-12 cells, and interference of circ_0001679 restrained LPS-induced apoptosis and production of pro-inflammatory cytokines by targeting the miR-338-3p/DUSP16 network.…”
Background: Sepsis-associated acute lung injury (SA-ALI) is a serious threat to human health. A growing body of evidence suggested that circular RNAs may be involved in ALI progression. The aim of this study was to investigate the effect and mechanism of circ_0001226 on lipopolysaccharide (LPS)–induced BEAS-2B cells. Methods: BEAS-2B cells were stimulated with LPS to establish a SA-ALI cell model. The expression of circ_0001226, miR-940, and transforming growth factor beta receptor II (TGFBR2) were monitored by quantitative real-time polymerase chain reaction. Cell proliferation and apoptosis were evaluated by the Cell Counting Kit-8, 5-ethynyl-2′-deoxyuridine assay, and flow cytometry. The levels of interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α were calculated by enzyme-linked immunosorbent assay. Western blot was implemented to test the protein levels of PCNA, Bax, and TGFBR2. Dual-luciferase reporter assay and RNA pull-down assay were adopted to investigate the interaction between circ_0001226 and miR-940, as well as TGFBR2 and miR-940. Results: The levels of circ_0001226 and TGFBR2 were elevated, and miR-940 was decreased in SA-ALI serum specimens and LPS-evoked BEAS-2B cells. Besides that, circ_0001226 interference contributed to cell proliferation and restrained apoptosis and inflammation in LPS-induced BEAS-2B cells. Mechanically, circ_0001226 worked as a molecular sponge of miR-940 to regulate TGFBR2 expression. Conclusion: Circ_0001226 deficiency weakened LPS-mediated proliferation inhibition and inflammatory processes in BEAS-2B cells by binding miR-940 and regulating TGFBR2.
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