ArticleBMC endocrine disorders2025
The predictive function of miR-122-5p and its action mechanism by regulating PKM2 in metabolic syndrome.
Article in BMC endocrine disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Pan-cancer analysis and experimental validation identify CYP19A1 as a prognostic biomarker and oncogenic driver associated with tumor immune microenvironment regulation in gastrointestinal cancers.Discover oncology · 2026Article
- Exploring the role of microRNA-155 as a biomarker and regulatory modulator of target genes in metabolic syndrome.SAGE open medicine · 2026Review
- Exogenous glucocorticoid dose impacts circulating microRNA expression in patients with adrenal insufficiency due to 21-hydroxylase deficiency.Frontiers in endocrinology · 2026Article
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Authors and funding
5 authors.
Funding
Abstract
backgroundObesity will cause metabolic syndrome (Mets) easily, and its pathogenesis is not completely clear.
aimTo probe into the predictive value of miR-122-5p and its regulatory mechanism in Mets.
methodThe predictive effect of miR-122-5p on Mets was evaluated by constructing a Receiver Operating Characteristic (ROC) curve. The target genes of miR-122-5p were predicted using the ENCORI/starBase and TargetScanHuman databases, and pyruvate kinase M2 (PKM2), closely related to Mets, was screened by GO and KEGG analysis. The roles of miR-122-5p/PKM2 in insulin resistance (IR) were explored by treating the human normal liver cells (HLCs) with palmitic acid (PA) to induce the IR model. The effects of miR-122-5p/PKM2 on glucose metabolism (GM) of HLCs were evaluated by detecting the production of pyruvic acid, lactic acid, and ATP.
resultsMiR-122-5p was highly expressed in obese people and Mets patients, and its predicted AUC for Mets was 0.876. In HLCs transfected with wild-type PKM2 luciferase vector (PKM2-wt), luciferase activity was attenuated by the miR-122-5p mimic and enhanced by its inhibitor. The expression of PKM2 was inhibited by the miR-122-5p mimic and up-regulated by its inhibitor. The miR-122-5p mimic enhanced PA-induced IR and inhibited the GM of HLCs, which were reversed by overexpression of PKM2. The miR-122-5p inhibitor exerted the opposite effects of its mimic, which were also reversed by silencing of PKM2.
conclusionMiR-122-5p, a risk factor for Mets, mediated the IR and abnormal glucose metabolism of HLCs by negatively regulating PKM2. CLINICAL TRIAL NUMBER: Not applicable.
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