MIR30A (MicroRNA 30a)

Several EMT-related miRNAs show consistent associations with invasion, metastasis, peritoneal dissemination, prognosis, and chemoresistance, and many are detectable in circulation. Overall, EMT-related miRNAs orchestrate gastric cancer cell plasticity and tumor-microenvironment crosstalk and represent promising biomarker and therapeutic candidates that warrant validation in prospective, subtype-stratified, and translational studies.

EC-derived Apo-EVs demonstrated excellent capacity to promote EPCs differentiation and angiogenesis both in vitro and in vivo, the mechanism is associated with miR-30a-5p within the vesicles inhibiting PML and activating the EGFR/PI3K/AKT/VEGF signaling pathway. This finding provides a new perspective for revealing the role of EC-derived Apo-EVs in tissue repair and offers potential strategies for the treatment of related diseases.

Ingenuity Pathway Analysis (IPA) revealed that miR-16-5p and other miRNAs with seed AGCAGCA formed the largest interaction network in GBM, while disease enrichment analysis using Database for Annotation, Visualization, and Integrated Discovery (DAVID) confirmed that the 1000 predicted mRNA targets of DE-miRNAs in GBM were disease relevant. Collectively, these findings identify a robust panel of CSF-derived miRNAs capable of distinguishing IDH-mutant gliomas, GBM, and non-tumor states, supporting the potential of EV-miRNAs as minimally invasive biomarkers for the molecular characterization of diffuse gliomas.

The results emphasizes that EGCG has strong binding affinity towards YWHAZ, revealing that miR-30a-EGCG targets TNBC synergistically through cell-cycle-mediated pathways. The findings give rational support for miRNA-guided phytochemical-based TNBC therapeutic development.

In particular, strategies that restore or inhibit miRNA activity using mimics or antagomiRs show promise in improving drug sensitivity and complementing current treatment options. Overall, emerging evidence supports the integration of miRNA profiling into precision oncology for SCLC, with the aim of refining diagnosis, risk assessment and therapeutic decision-making.

Given the small sample size (n = 10), these findings should be interpreted as preliminary and hypothesis-generating, warranting validation in larger cohorts. Nevertheless, findings support household testing, remediation at ≥100 Bq/m3, and integrated exposure studies considering PM2.5 co-exposures.

miR-30a-5p participates in regulating the proliferation of Wilms tumor cells by suppressing the CCNE2/p-Rb/E2F1 axis.

STRING analysis identified IKBKB as a central hub in the PPI network, while GO enrichment highlighted immune regulation, apoptosis, and NF-κB signaling. These findings demonstrate that adalimumab modulates NF-κB activity in keratinocytes through coordinated regulation of gene, protein, and miRNA expression, providing mechanistic insight into TNF-α blockade in psoriasis.

These alterations reflect both the suppression of upstream Hippo activation and activation of downstream oncogenic effectors across all subtypes. Our findings reveal a conserved Hippo dysregulation program in breast cancer, highlighting subtype-independent Hippo-related genes and their miRNA regulators as potential universal biomarkers and therapeutic targets, complementing subtype-specific treatment strategies.

A literature search was manually curated and conducted on PubMed for studies published mainly in the last decade and evaluating the effects of metformin, sodium-glucose cotransporter-2 (SGLT2) inhibitors, peroxisome proliferator-activated receptor gamma (PPARγ) agonists, glucagon-like peptide 1 (GLP-1) receptor agonists, and fatty acid oxidation inhibitors on ncRNA expression in the context of cardiovascular fibrosis... Metabolic modulators exert anti-fibrotic effects partly through ncRNA regulation, offering novel therapeutic strategies and potential biomarkers for cardiovascular fibrosis in cardiometabolic disease. Targeting metabolic-ncRNA crosstalk may enable more precise and synergistic interventions for preventing or reversing pathological remodeling.