MIR139 (MicroRNA 139)

Notable differences in miRNA expression profiles were revealed for the patients with brain metastases from lung cancer, suggesting the role of the selected miRNAs in cancer metastasis to the CNS. However, while our analysis provides exploratory insights, the findings should be interpreted with caution and require validation in larger, independent cohorts before any clinical or translational implications can be established.

The overexpression of miR-139-3p in BC cells enhanced cisplatin, olaparib, and irradiation (IR) sensitivity. The diagnostic model based on the four circulating miRNAs could serve as a tool for the liquid biopsy of BC. Targeting the miR-139-3p/RPA2 axis may have potential in modulating the DNA damage pathway in BC.

WFC shows promise in benefiting patients with stage II and III GC. Through its modulation of the miR-139-5p/CXCR4 axis, WFC serves as a potent inhibitor of angiogenesis, potentially enhancing the effectiveness of chemotherapy while reducing GC recurrence and metastasis.

The transfer-learned model ultimately achieves a high classification accuracy of 91.5% and a sensitivity of 92.2% on the clinical serum test set. We envision that the approach offers a cost-effective solution for high-accuracy liquid biopsy with limited samples.

MiR-139 inhibits lung cancer cell migration and invasion by targeting ERBB2, suppressing Rac1 activity, and downregulating NF-κB signaling. Its downregulation promotes metastasis through the ERBB2/Rac1/NF-κB axis.

Mechanistically, miR-182-5p enhanced metastasis via ANLN and PDE4D regulation, whereas miR-203, miR-150-5p, and miR-139-5p suppressed metastasis through PDE4D, NEGR1, and ATP11A pathways, respectively. These results highlight the opposing roles of miR-182-5p and the tumor-suppressive miRNAs in CRC metastasis and suggest their potential as biomarkers and therapeutic targets.

In the training and validation sets, the area under the curve of the 4-miRNA panel was 0.909 and 0.942, respectively. These findings suggest that the serum glycosylated exosomal 4-miRNA panel developed using the GlyExo-Capture approach may serve as a promising strategy for liquid biopsy-based early detection of LUAD.

This study, for the first time, elucidates the mechanism by which miR-139-5p suppresses HCC progression through targeting SMOX to inhibit the AKT-mTOR pathway and EMT. These findings suggest that both miR-139-5p and SMOX could serve as potential therapeutic targets for HCC treatment.

Therefore, circ_0006174, regulated by METTL3-mediated m6A methylation, promoted the progression of TNBC through the miR-3139/PD-L1 axis. This study was the first to validate the circ_0006174 as a novel m6A-modified circRNA as well as the circ_0006174/miR-3139/PD-L1 axis as a potential target for TNBC.

The miRNA-mRNA interactions were validated using real-time PCR in independent patient cohorts. This study revealed a complex molecular landscape of mCLM within the hepatic microenvironment and novel miRNA-mRNA interactions with potential prognostic and therapeutic implications.

Moreover, the restoration of miR-139-5p by its re-introduction through miR-139-5p mRH-NPs is functionally active in cellular models of TNBC (MDA-MB-231 and HCC-1395) reducing their clonogenic ability, increasing their sensitivity to the chemotherapeutic agent Doxorubicin (Dox) and impairing their migratory ability. Thus, this study contributes in addressing the critical challenges of miRNA-based therapy and proposes HSAcys nanoparticle-mediated delivery of miRNAs as a potential adjuvant strategy to enhance therapeutic efficacy in cancer treatment.

These effects were all partially attenuated by silencing of miR-139-5p. RMST can aggravate neuroinflammation and apoptosis in microglia after TBI and thereby affect neurological dysfunction by regulating miR-139-5p.