Immunological investigations · 2026
Reduced miR-193a-3p Modulates Cell Proliferation and Apoptosis in Inflammatory Bowel Disease via Targeting ETS1.
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Cheng Hailin, Xiao Lei, Xu Tao
Аннотация
BACKGROUND: Multiple findings have demonstrated that microRNAs (miRNAs) have a profound impact on inflammatory bowel disease (IBD) pathogenesis. This research was conceived to elucidate the regulatory function of miR-193a-3p in IBDby targeting ETS proto‑oncogene 1 and explore its potential diagnostic value.
METHODS: Expression of miR-193a-3p was determined by reverse transcription quantitative real‑time polymerase-chain reaction (RT‑qPCR). Cell viability, apoptosis, and inflammatory responses were measured in lipopolysaccharide (LPS)-stimulated human normal colonic epithelial FHC cells using the cell counting kit‑8 (CCK‑8) assay, flow cytometry, and enzyme‑linked immunosorbent assay (ELISA), respectively. The dual-luciferase reporter's assay verified the targeting relationship.
RESULTS: miR-193a-3p was downregulated whereas ETS1 was upregulated in patients with inflammatory bowel disease (IBD). Its expression was negatively correlated with IBD severity in both ulcerative colitis (UC) and Crohn's disease (CD). In vitro, elevated miR-193a-3p alleviated LPS-induced inflammation and apoptosis and promoted cell proliferation. A negative regulatory relationship between miR-193a-3p and ETS1 was validated experimentally. miR-193a-3p overexpression inhibited LPS-mediated upregulation of ETS1. In addition, ETS1 overexpression suppressed cell proliferation and facilitated inflammation and cell apoptosis.
CONCLUSION: miR-193a-3p was involved in the pathogenesis of IBD by directly targeting ETS1.
METHODS: Expression of miR-193a-3p was determined by reverse transcription quantitative real‑time polymerase-chain reaction (RT‑qPCR). Cell viability, apoptosis, and inflammatory responses were measured in lipopolysaccharide (LPS)-stimulated human normal colonic epithelial FHC cells using the cell counting kit‑8 (CCK‑8) assay, flow cytometry, and enzyme‑linked immunosorbent assay (ELISA), respectively. The dual-luciferase reporter's assay verified the targeting relationship.
RESULTS: miR-193a-3p was downregulated whereas ETS1 was upregulated in patients with inflammatory bowel disease (IBD). Its expression was negatively correlated with IBD severity in both ulcerative colitis (UC) and Crohn's disease (CD). In vitro, elevated miR-193a-3p alleviated LPS-induced inflammation and apoptosis and promoted cell proliferation. A negative regulatory relationship between miR-193a-3p and ETS1 was validated experimentally. miR-193a-3p overexpression inhibited LPS-mediated upregulation of ETS1. In addition, ETS1 overexpression suppressed cell proliferation and facilitated inflammation and cell apoptosis.
CONCLUSION: miR-193a-3p was involved in the pathogenesis of IBD by directly targeting ETS1.