MIR363 (MicroRNA 363)

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 approach combines high sensitivity, wide dynamic range, quantitative precision, and spatial resolution, allowing amplification-free monitoring of miRNA expression in live cells. This versatile platform provides a powerful tool for intracellular biosensing, with potential applications in live-cell diagnostics, therapeutic response profiling, and studies of single-cell gene regulation.

Circulating miRNA profiling showed upregulation of inflammation-associated miRNAs (miR-21-5p, miR-150-5p, miR-142-3p, miR-363-3p), linked through bioinformatic analysis to immune dysregulation, intestinal cancer, and neurotoxicity. Overall, these results indicate that low-dose exposure to pollutant mixtures can induce subtle but biologically relevant immune and epithelial changes, emphasizing the importance of mixture-based approaches in environmental risk assessment.

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The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 16: 1603‑1611, 2017; DOI: 10.3892/mmr.2017.6759].

Therefore, the tracking of glioma stage and response to anticancer therapy is associated with various miRNAs. The objective of this review is to provide a comprehensive assessment of the role of miRNAs in glioma cancer development.

PAL upregulates miR-363-3p expression, promotes the interaction between AURKA 3'UTR mRNA and miR-363-3p, impedes AURKA mRNA translation into AURKA protein, thereby inhibiting colorectal cancer cell proliferation and migration, and suppressing the initiation and progression of colorectal cancer. These results expand the understanding of the regulatory mechanisms by which PAL influences colorectal cancer development, and may provide new potential targets for colorectal cancer diagnosis and therapy.

According to the Gene Expression Profiling Interactive Analysis (GEPIA) database results, the target genes AFAP1L1, GPT2, PPP1R12B, PRNP and SGIP1 in the three-miRNA panel were good candidates. Our three-miRNA panel (hsa-miR-20b-5p, hsa-miR-200b-3p and hsa-miR-106a-5p) is anticipated to be a promising non-invasive biomarker for NPC screening and diagnosis.

Furthermore, miR-363-3p overexpression restored sorafenib sensitivity, whereas upregulated DUSP10 expression promoted sorafenib resistance in sorafenib-resistant cell lines. In conclusion, the lncRNA EMS/miR-363-3p/DUSP10 axis regulates sorafenib resistance in RCC, and these molecules are promising biomarkers and therapeutic targets for patients with sorafenib-resistant RCC.

Ultimately, miR-363-3p decreased the responsiveness of breast cancer cells to TAM by targeting and suppressing PTEN through a mechanism associated with the PI3K-Akt pathway. Therefore, these results suggest that miR-363-3p-dependent PTEN expression contributes to the mechanisms underlying breast cancer endocrine resistance.

The latter group of cases with a recessive genetic pattern (GG vs. GC+ CC) showed enhanced susceptibility to promoting PDAC (OR = 1.7; 95% CI: 1.2-2.9; p = 0.04). Our findings indicate that genetic variation in CDKN2A was linked to the susceptibility of extending PDAC, suggesting the need for additional research in a broader, multi-center context to approve the possible significance of this gene as a novel indicator for the stratification of PDAC.