MIR485 (MicroRNA 485)

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.

Preliminary results indicate that the biomarker panel combining serum miR-485-3p levels with CDUS parameters shows diagnostic potential for PTC. In vitro experiments confirmed the potential of the miR-485-3p/GCNT4 axis in modulating the malignant behavior of PTC cells.

ROC curve analysis showed that both miRNAs demonstrated good diagnostic efficacy for pneumoconiosis, with AUC values of 0.9563 and 0.8876, respectively. These results provide novel insights into the complex ceRNA regulatory network involved in silicosis pathogenesis and suggest potential early, non-invasive diagnostic biomarkers.

[This retracts the article DOI: 10.1155/2021/1281031.].

Significantly upregulated LINC00265 is a biomarker for the diagnosis of breast cancer, and LINC00265 binds to miR-485-5p to mediate tumor progression.

The link between miR-485-5p and GAS5 was established in MSU-induced THP-1 macrophages. In summary, GAS5 alleviated MSU-induced excessive inflammation in THP-1 macro- phages by targeting miR-485-5p, suggesting that GAS5 is a potential diagnostic biomarker for AGA treatment.

In addition, we show that there are pairs of known miRNA WTs differing only by disease-related point mutations outside the seed region and exhibit very different SS. These pairs include hsa-miR-1269a-hsa-miR-1269b, and hsa-miR-3689a-3p-hsa-miR-3689b-3p.

RAPGEFL1 regulates the Rap signaling pathway, controlling adhesion, migration, polarity, and metabolism to maintain cellular and tissue homeostasis. Its dysregulation is linked to various diseases, highlighting its potential as a therapeutic target.

MSCs enhance the stemness and chemoresistance of GC cells by secreting lncRNA NKILA, which promotes fatty acid oxidation through STAT3 activation. NKILA modulates the miR-485-5p/STAT3 axis, thereby increasing energy metabolism and supporting cancer stem cell properties. Targeting NKILA or the miR-485-5p/STAT3 pathway offers potential therapeutic strategies to overcome chemoresistance in GC.

Mechanistically, PPARGC1A/PGC-1α is post-transcriptionally repressed by miR-485-3p in cardiomyocytes, leading to the inhibition of mitochondrial complex I subunits and ATP synthesis. Taken together, our findings reveal for the first time that cancer can aggravate cardiac injury and mitochondrial dysfunction by releasing miR-485-3p-enriched extracellular vesicles derived from cancer cells.

Inhibiting LINC00365 may suppress the proliferation, migration and invasion abilities of TC cells. LINC00365 may be a potential prognostic indicator for TC, and LINC00365 may promote tumor growth and metastasis of TC by inhibiting miR-485-5p expression.