MIR374A (MicroRNA 374a)

The ISL demonstrated potent anticancer effects by: (1) Inducing apoptosis and autophagy via mechanistic target of rapamycin (mTOR) inhibition and disruption of arachidonic acid pathways; (2) modulating microRNAs (miRs; e.g., miR-374a, miR-200c) to suppress epithelial-mesenchymal transition (EMT); (3) altering hormone receptor [HR; ERα, breast cancer type 1 susceptibility protein (BRCA1)] expression and inhibiting phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mTOR signaling; and (4) reducing angiogenesis [vascular endothelial growth factor (VEGF)/hypoxia-inducible factor-1 alpha (HIF-1α) suppression] and inflammation [cyclooxygenase-2 (COX-2)/nuclear factor-kappa B (NF-κB) inhibition]...However, clinical trials are urgently needed to validate its efficacy, safety, and optimal delivery strategies in patients. Future research should prioritize translational studies and combinatorial therapies to bridge the gap between bench and bedside.

TRAF3IP2-AS1/miR-374a-5p/SEL1L/RPL6 pathway in HCC cells promoted DDR and HCC progression. Our data identify the role and mechanism of TRAF3IP2-AS1 in HCC and imply treatment targets for HCC.

miR-374a-5p acts in PCa by inhibiting cell proliferation, migration, and invasion. Consequently, miR-374a-5p has potential to act as a prognostic biomarker and a target for clinical therapeutic intervention in PCa.

In summary, high expression of Lnc-FTX possesses clinical value in predicting poor prognosis in HCC. As an oncogene, it promotes the malignant functions of HCC through the RBMX/Lnc-FTX interaction and the Lnc-FTX/miR-374a-3p/HMGB1 signaling pathway.

This study suggests that the specific expression of miRNA-1296-5p, miR-499a-5p, miR-374a-5p and miR-370-3p in the serum exosomes of LC, which has diagnostic potential. And the combination of miRNA-1296-5p, miR-499a-5p and miR-370-3p with CEA can further enhance this potential.

Our study reveals novel molecular signatures linking gut microbiome and host transcriptome in HT, providing new insights into the disease pathogenesis. These findings not only enhance our understanding of the gut-thyroid axis but also suggest potential new directions for therapeutic interventions in HT.

The findings suggest that the miR-374a‑5p/ANLN signaling axis potentially modulates the advancement of OSCC, and miR-374a‑5p may serve as potential therapeutic targets of oral cancer.

Notably, only two DEGs were associated with the response to trichostatin A: ARP2 actin-related protein 2 homolog (ACTR2) and MEF2C; ACTR2 garnered particular interest...The dual-luciferase reporter (DLR) assay demonstrated that the fluorescence activity of ACTR2-WT was significantly inhibited by the miR-374a-5p mimic sequence (P<0.05), confirming the presence of a targeted regulatory relationship between ACTR2 and miR-374a-5p. These findings offer novel insights for future research directions in the diagnosis and treatment of OS.

ILN emerges as a promising natural option, offering therapeutic advantages with minimal side effects. However, it is important to note that current research on ILN is primarily limited to preclinical models, underscoring the need for further investigation to validate its potential efficacy.

Mechanistically, miR-374a-5p regulates the distribution of ZO-1 and occludin in endothelial cells by targeting ADD3, increasing vascular permeability and promoting LM. Implications: These results suggest that serum NSCLC-derived EVs miR-374a-5p is involved in premetastatic niche formation by regulating the permeability of BBB to promote NSCLC-LM, and can be used as a blood biomarker for the diagnosis and prognosis of NSCLC-LM.

MicroRNA-374a-5p (miR-374a-5p) and microRNA-374b-5p (miR-374b-5p) were identified as inhibitors of ANXA1 expression and PI3K/AKT pathway activity, thereby inhibiting macrophage M2 polarization. Furthermore, miR-374a-5p and miR-374b-5p were observed to suppress PTC cell proliferation through their regulatory action on ANXA1. Our study suggests that miR-374a/b-5p inhibits PTC cell growth by blocking the macrophage M2 polarization induced by exosomal ANXA1.

Especially, among the 57 lung cancer-associated miRNAs, BPDE-Alb adducts were significantly related to miR-17-3p, miR-20a-3p, miR-135a-5p, miR-374a-5p, miR-374b-5p, miR-423-5p and miR-664a-5p, which could in turn mediate a separate 42.2%, 33.0%, 57.5%, 36.4%, 48.8%, 32.5% and 38.2% of the relationship of BPDE-Alb adducts with the risk of lung cancer. Our results provide non-invasion biomarker candidates for lung cancer, and highlight miRNAs dysregulation as a potential intermediate mechanism by which BaP exposure lead to lung tumorigenesis.