ArticleMolecular biology reports2025
Dysregulation of hsa-mir-10a-5p modulates RNF186 and contributes to ulcerative colitis pathogenesis.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMicroRNAs (miRNAs) are post-transcriptional regulators that influence gene expression and dysregulation has been linked to the pathogenesis of ulcerative colitis (UC). The current study investigated the regulatory axis between hsa-mir-10a-5p and RNF186 in UC inflammation.
methodsRNF186 was identified as a target of hsa-mir-10a-5p by bioinformatics prediction and dual-luciferase reporter assay. A UC cell model was established by lipopolysaccharide (LPS) stimulation of HT-29 intestinal epithelial cells. Gain-of-function (overexpression) and loss-of-function (knockdown) experiments targeting hsa-mir-10a-5p and RNF186 were performed to assess function and mRNA and protein expression were measured by quantitative real-time PCR (qRT-PCR) and western blotting. Apoptosis was quantified by flow cytometry.
resultshsa-mir-10a-5p was shown to bind to the 3’UTR of RNF186 by dual-luciferase assay and a negative correlation shown between the expression of hsa-mir-10a-5p and RNF186 in a UC model. hsa-mir-10a-5p overexpression downregulated RNF186 expression, reduced pro-inflammatory cytokines, TNF-α, IL-6, and attenuated apoptosis. hsa-mir-10a-5p knockdown upregulated RNF186 expression and exacerbated inflammatory responses. RNF186 knockdown produced a similar anti-inflammatory effect to that observed with hsa-mir-10a-5p overexpression. RNF186 overexpression increased inflammatory damage.
conclusionhsa-mir-10a-5p negatively regulated RNF186 and modulated the inflammation characteristic of UC. The hsa-mir-10a-5p/RNF186 axis may be a novel therapeutic target for UC.
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