MIR3613 (MicroRNA 3613)

The miR-3613-5p-XPO6 axis may act as a LC therapeutic target, and novel therapeutic strategies for LC could be developed based on this axis.

This is the first study integrating miRNA expression with clinicopathological features in a logistic model for breast cancer prognosis. While further validation is needed, our model shows promise as a prognostic tool across all breast cancer subtypes. In silico pathway enrichment analysis highlights miR-3613-5p and miR-3916 as critical regulators of metastasis development, underscoring the need for further investigation.

MiR-3613-3p negatively regulated EphA7 expression levels, and overexpressing miR-3613-3p reversed the reduction of the apoptosis rate and increase of cell proliferation caused by overexpression of EphA7. In this research, we identified that high expression levels of miR-3613-3p were associated with a better prognosis and EphA7 was negatively regulated by miR-3613-3p to inhibit the development of glioma.

The coexistence of truncating and missense variants further highlights the need for mechanistic validation, and integrative pathway analysis to identify synthetic lethal targets and improve the therapeutic strategies. Integrating ARID1A into precision oncology is a promising approach for improving the diagnostic, prognostic, and treatment modalities for patients with ARID1A-deficient cancers.

There was a significant correlation between the miR-3613-3p expression and the clinical stage of GC (p = 0.049). ROC analysis revealed that combining miR-106a-5p, miR-129-5p, miR-1301-3p, and miR-647 improves diagnostic and prognostic properties of the potential panel of markers.

The results from this pilot transcriptomic analysis (mRNA and miRNA) indicate that exposure to NPs contributes to immune system deregulation and alters the pathways related to cancer. Therefore, the use of protective equipment, as well as obtaining more data by additional research, is highly recommended.

Our findings suggest that differentiation of cell subpopulations is regulated by specific miRNAs. Furthermore, miRNA-based strategies may be developed for immunotherapeutic treatments of AML.

Our findings provide the first evidence that miR-3613-5p facilitates CAG progression toward GC via negative regulation of AQP4. These results highlight miR-3613-5p as a promising biomarker and therapeutic target, suggesting antagomiR-3613-5p as a potential novel strategy to prevent gastric carcinogenesis.

To validate predicted target pairs miR-129-5p/ARID1A and miR-3613-3p/ARID1A, in vitro experiments on cancer cell lines were conducted. The obtained results suggest a complex role of ARID1A, miR-129-5p and miR-3613-3p in GC and potential regulation of ARID1A expression by both miRNAs.

The study findings encourage us to hypothesize that the aforementioned miRNAs may contribute to the predominance of aGVHD, particularly low-grade cutaneous aGVHD.

Our findings indicated that miR-3613-3p plays an important role in CRC by targeting the TGF-β/SMAD signaling pathway and could be considered as a new candidate for further therapy investigations.

Through an unbiased screening of EV-derived sncRNAs, we characterize miRNAs and piRNAs in the EVs cargo as potential biomarkers and modifiers of diverse IIM phenotypes.