ArticlePloS one2024
MiR-27a inhibits the growth and metastasis of multiple myeloma through regulating Th17/Treg balance.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Comparative Molecular Insights and Computational Modeling of Multiple Myeloma and Osteosarcoma.International journal of molecular sciences · 2026Review
- Effect of Topical Corticosteroid Treatment on microRNA Expression in Infants with Atopic Dermatitis.JID innovations : skin science from molecules to population health · 2025Article
- Development and validation of a multiple myeloma diagnostic model based on systemic lupus erythematosus-associated genes and identification of specific genes.Discover oncology · 2025Article
- Significance of the peripheral blood Treg/Th17 ratio as a prognostic immune biomarker in newly diagnosed multiple myeloma and its correlation with 1q21 gain/amplification.Frontiers in immunology · 2025Article
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Authors and funding
6 authors.
Funding
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Abstract
backgroundThe imbalance between T helper 17 (Th17) and T regulatory (Treg) cells plays a key role in the progression of multiple myeloma (MM).
methodsThe gene expression profiles of MM were acquired and examined from the Gene Expression Omnibus (GEO) database (GSE72213). Our research involved experimental investigations conducted using the MOPC-MM mouse model. Dysregulation of Treg and Th17 cells was evaluated through flow cytometry, while the levels of inflammatory factors were measured using the enzyme-linked immunosorbent assay. Cell proliferation was gauged using the Cell Counting Kit-8 assay, and cell apoptosis was quantified via flow cytometry. Cell metastasis capabilities were determined by conducting transwell assays. To confirm the relationship between miR-27a and PI3K, a dual-luciferase reporter assay was employed. Finally, proteins associated with the PI3K/AKT/mTOR signaling pathway were assessed using western blotting.
resultsMiR-27a exhibited reduced expression levels in MM. Moreover, it exerted control over the equilibrium of Th17 and Treg cells while reducing the expression of inflammatory mediators such as TGF-β1 and IL-10 in an in vivo setting. Elevated miR-27a levels led to the inhibition of cell viability, colony formation capacity, migratory and invasive traits in an in vitro context. The PI3K/AKT/mTOR signaling pathway was identified as a direct target of miR-27a and could reverse the effects induced by miR-27a in MM cells. Notably, PI3K was directly targeted by miR-27a.
conclusionsOur study revealed that miR-27a inhibited MM evolution by regulating the Th17/Treg balance. Inhibition of the PI3K/AKT/mTOR signaling pathway by miR-27a may play a potential mechanistic role.
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