MIR126 (MicroRNA 126)

Experimental results demonstrate a picomolar detection limit for miRNA-126 and excellent performance in serum samples. Overall, this study provides a promising strategy for sensitive and specific early cancer screening and point-of-care diagnostics.

[This retracts the article DOI: 10.3727/096504016X14685034103879.].

The publicly available microarray datasets, including GSE39001, GSE9750, GSE7803, GSE6791, GSE63514, and GSE52903 in combination with bioinformatics database predictions, were used to identify differential expression genes, potential biomarkers, and therapeutic targets for cervical cancer; additionally, we undertook bioinformatic analysis to determine gene ontology and possible miRNA targets related to our DEGs...Interestingly, hub proteins KIF4A, NUSAP1, BUB1B, CEP55, DLGAP5, NCAPG, CDK1, MELK, KIF11, and KIF20A were found to be potentially regulated by several miRNAs, including miR-107, miR-124-3p, miR-147a, miR-16-5p, miR-34a-5p, miR-34c-5p, miR-126-3p, miR-10b-5p, miR-23b-3p, miR-200b-3p, miR-138-5p, miR-203a-3p, miR-214-3p, and let-7b-5p. The relationship between these genes highlights their potential as candidate biomarkers for further research in treatment, diagnosis, and prognosis.

We identified several miR polymorphisms and distinct haplotypes associated with reduced PCa risk in a sample of the Iranian population. These findings pave the way for optimized PCa management and provide a better understanding of its pathophysiology.

A competing endogenous RNA (ceRNA) network involving miRNAs (e.g., miR-16-5p, miR-126-5p) and lncRNAs (e.g., AC008124.1, AC064799.2, AGAP11) potentially modulates their expression. This study identifies seven novel candidate biomarkers dysregulated in endothelial cells under combined BCR-ABL and exosomal stimulation, shedding light on the molecular crosstalk between leukemic cells and the vascular niche.

Herein, we analyze the LAT1/SLC7A5-mediated uptake of several essential AAs in FPR2-stimulated CaLu-6 and HCC1937 cells and prove: (i) the redox regulation of both LAT1/SLC7A5 and 4F2hc/SLC3A2/CD98, which form a heterodimer on the plasma membrane; (ii) the redox activation of the mTOR pathway and, in turn, of S6K1 and 4E-BP1, which stimulate protein synthesis; (iii) c-Myc and miR-126 regulation, which control LAT1/SLC7A5 synthesis at the transcriptional and post-transcriptional level, respectively. These findings provide new approaches for the development of novel therapeutic strategies for the treatment of human cancers.

CAFs-derived exosomal miR-3126-5p enhanced glycolysis of NSCLC cells via targeting KLF13. KLF13 led to transcriptional inhibition of SH2B1 in NSCLC cells. SH2B1 interplayed with IRS1 to facilitate glycolysis of NSCLC cells. IRS1 promoted glycolysis of NSCLC cells via the activation of PI3K/AKT pathway.

Leukemic stem cells (LSCs) in acute myeloid leukemia (AML) depend on oxidative phosphorylation (OXPHOS) sustained by fatty acid oxidation (FAO) and mitochondrial fusion (mitofusion). In vivo, miRisten potentiated the VEN/azacitidine (AZA) regimen, an FDA-approved therapy for older or unfit AML patients, significantly prolonging survival in patient-derived xenograft models. VEN/miRisten combination also reduced LSC burden and restored VEN sensitivity, establishing miR-126 inhibition as a transformative therapeutic strategy in AML.

Preclinical studies using both systemic and intranasal administration of MSC-Exos have demonstrated significant therapeutic benefits. In murine models of allergic airway inflammation, treatment with MSC-Exos resulted in reduced eosinophilic infiltration, decreased serum IgE levels, and suppression of mucus hypersecretion. These effects were accompanied by enhanced secretion of IL-10 and TGF-β, two key anti-inflammatory cytokines that contribute to an immunosuppressive microenvironment.9 Collectively, these findings indicate that MSC-Exos can recapitulate many of the beneficial immunomodulatory effects of MSC therapy while avoiding several of the risks associated with live cell transplantation, such as immune rejection or tumorigenicity. A major advantage of MSC-Exos therapy is its cell-free and safer nature, avoiding risks associated with stem cell transplantation. Due to their nanoscale size, lipid bilayer structure, and endogenous cargo, MSC-Exos can efficiently deliver regulatory molecules to target tissues, outperforming many synthetic nanocarrier systems. Nevertheless, translating these promising preclinical findings into clinical practice requires overcoming several challenges, including standardized isolation and characterization protocols, scalable GMP-compliant production, dose optimization, and rigorous long-term safety evaluation.

MiR-126-5p, miR-150-5p, miR-214-3p, and miR-452-5p all showed a decrease in expression at at least one timepoint following splenectomy. These miRNAs have been previously shown to have roles in angiogenesis and pathways known to be involved in the pathogenesis of hemangiosarcoma and may be prospective targets for a minimally invasive diagnostic panel for the presence of splenic hemangiosarcoma.

If a mass is not hemangiosarcoma, owners may be more likely to proceed with surgery rather than euthanasia. Knowing that a mass is hemangiosarcoma will provide information to owners on the need for adjuvant therapy following surgery.

Functional studies confirmed that miR-21-5p mediates these effects by downregulating PTEN and PDCD4, and by upregulating MMP9 expression. Our findings show that NSCLC-PE-EVs promote malignant phenotypes in lung cancer cells via the transfer of miR-21-5p.