MIR455 (MicroRNA 455)

This study investigates the therapeutic efficacy of sacubitril/valsartan in a bleomycin-induced rat model of pulmonary fibrosis. Additionally, sacubitril/valsartan treatment resulted in a notable reduction in pulmonary levels of transforming growth factor-β (TGF-β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), indicating attenuation of both fibrotic and inflammatory responses. Collectively, these findings suggest that sacubitril/valsartan mitigates pulmonary fibrosis through modulation of the SNHG-16/miR-455 axis and inhibition of the Notch-2/Smad-3/TGF-β signaling cascade, highlighting its potential as a promising therapeutic strategy for the management of pulmonary fibrosis.

Moreover, distinct miRNA expression patterns are correlated with tumor aggressiveness, metastatic potential, and the risk of recurrence, supporting their integration with conventional histopathological and molecular parameters for improved patient stratification. Overall, miRNAs represent a powerful class of biomarkers and potential therapeutic targets in EC, with increasing translational relevance in precision oncology.

The specific isoform miR-455-5p 0|1 likely exerts a tumour-suppressive role, potentially through a non-canonical regulatory interaction with SP100. These findings unveil isomiR-mediated regulation as a critical layer of molecular complexity in Wilms' tumour, offering new insights for prognostic stratification.

Mutational analysis further highlighted the significance of KRAS G12C, G12V, and G12D mutations, which were common between RCC and pancreatic metastasis. Our study provides critical insights into the statistically significant associations between metabolic disorders and malignancies, emphasizing the potential of tailored therapies alongside shared therapies in managing RCC and its progression to pancreatic metastasis.

The TNBC prognostic signature comprising four interferon genes (STXBP1, LAMP3, CD276, and POLR2F) was identified, with their expression significantly correlated with the infiltration abundance of multiple immune cells and the drug sensitivity of 30 diverse drugs (ARQ-680, Fluphenazine, and Chelerythrine, etc.). In the prognostic signature and the ceRNA axes, STXBP1, RBPMS-AS1, and FAM198B-AS1 were first reported as potential biomarkers of TNBC. These findings have the potential to provide new insights into the mechanisms driving TNBC tumorigenesis and development.

Two miRNAs-miR-449b and miR-455-3p-were common in both compartments, highlighting their translational potential as liquid biopsy surrogates of tumor biology. (4) We summarize functional evidence for leading tumor-suppressive (e.g., miR-205, miR-23b, miR-455-3p) and oncogenic (e.g., miR-21, miR-182, miR-449b) candidates, discuss their intersection with the androgen-receptor, TGF-β, WNT/β-catenin, and PI3K-AKT signaling, and outline outstanding requirements for the clinical qualification of miRNA panels in prostate cancer.

CD44, RHOC, HCN4, and MYH10 were identified as shared hub genes between Graves' disease and thyroid cancer, with functional roles in oncogenic pathways. Their diagnostic and therapeutic potential offers novel insights into thyroid disease pathogenesis.

However, in the six-miRNA combination, it was possible to distinguish low-risk PTMC from aggressive PTMC with an AUC of 0.763, sensitivity of 0.739, and the specificity of 0.727. A combination of six miRNAs presents the possibility of distinguishing between benign and PTMC and low-risk and aggressive PTMC with an acceptable AUC, sensitivity, and specificity.

This hydrogel "awakened" dormant SACC cells, suppressing their tumorigenic potential and leading to their eradication through sustained paclitaxel release in vivo. This approach presents a new therapeutic strategy for eliminating dormant tumor cells and reducing the risk of post-therapy cancer relapse.

Hsa_circ_0049271 promoted the secretion of senescence-associated secretory phenotypes, including IL1B, IL6, CXCL5, and MMP3. Hsa_circ_0049271 may enhance DDP treatment-induced cellular senescence to promote ESCC progression and chemoresistance through the miR-455-5p/ETS1 axis.

TB-II suppresses GC cell proliferation and induces apoptosis via the Nrf2/miR-455-3p/KLF6 pathway.

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.