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Background <p>The incidence of pediatric ulcerative colitis (UC) is increasing yearly, and it is urgent to explore precise diagnostic biomarkers and molecular mechanisms. This study aims to investigate the diagnostic value of miR-340-5p in pediatric UC and its molecular mechanism mediated through targeting <i>MAP3K2</i>.</p> Methods <p>Eighty-five pediatric UC patients and 50 healthy controls were enrolled. The expression levels of miR-340-5p and <i>MAP3K2</i> were detected by qRT-PCR, and Pearson’s correlation analysis was conducted. An in vitro model was established by inducing HT-29 cells with dextran sulfate sodium. The target was verified by dual-luciferase assay. Flow cytometry, ELISA, and oxidative stress detection were used to verify the cellular functions regulated by the miR-340-5p/<i>MAP3K2</i> axis.</p> Results <p>In pediatric patients with UC, miR-340-5p was significantly downregulated and negatively correlated with PUCAI, CRP, and ESR (<i>P</i> &lt; 0.0001). Additionally, the diagnostic area of miR-340-5p under the ROC curve was 0.908. Mechanistically, miR-340-5p directly interacts with <i>MAP3K2</i>, leading to suppressed expression of its mRNA and protein. Functional experiments revealed that miR-340-5p overexpression reversed DSS-induced exacerbated cell apoptosis, reduced levels of TNF-α, IL-6, IL-17, IL-1β, and MDA, and increased GSH. Conversely, the beneficial effects of miR-340-5p were attenuated by oe-<i>MAP3K2</i> overexpression.</p> Conclusions <p>miR-340-5p may serve as a diagnostic biomarker for pediatric UC and exerts its effects by targeting <i>MAP3K2</i> to regulate cell apoptosis, inflammatory responses, and oxidative stress.</p>

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The diagnostic value of miR-340-5p in pediatric ulcerative colitis and its molecular mechanism by targeting MAP3K2 to modulate intestinal epithelial cell dysfunction

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月19日

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  • Fanting Meng,
  • Xianlong Han,
  • Lingxia Ge,
  • Nan Guan

摘要

Background

The incidence of pediatric ulcerative colitis (UC) is increasing yearly, and it is urgent to explore precise diagnostic biomarkers and molecular mechanisms. This study aims to investigate the diagnostic value of miR-340-5p in pediatric UC and its molecular mechanism mediated through targeting MAP3K2.

Methods

Eighty-five pediatric UC patients and 50 healthy controls were enrolled. The expression levels of miR-340-5p and MAP3K2 were detected by qRT-PCR, and Pearson’s correlation analysis was conducted. An in vitro model was established by inducing HT-29 cells with dextran sulfate sodium. The target was verified by dual-luciferase assay. Flow cytometry, ELISA, and oxidative stress detection were used to verify the cellular functions regulated by the miR-340-5p/MAP3K2 axis.

Results

In pediatric patients with UC, miR-340-5p was significantly downregulated and negatively correlated with PUCAI, CRP, and ESR (P < 0.0001). Additionally, the diagnostic area of miR-340-5p under the ROC curve was 0.908. Mechanistically, miR-340-5p directly interacts with MAP3K2, leading to suppressed expression of its mRNA and protein. Functional experiments revealed that miR-340-5p overexpression reversed DSS-induced exacerbated cell apoptosis, reduced levels of TNF-α, IL-6, IL-17, IL-1β, and MDA, and increased GSH. Conversely, the beneficial effects of miR-340-5p were attenuated by oe-MAP3K2 overexpression.

Conclusions

miR-340-5p may serve as a diagnostic biomarker for pediatric UC and exerts its effects by targeting MAP3K2 to regulate cell apoptosis, inflammatory responses, and oxidative stress.