MIR489 (MicroRNA 489)

Both in vitro and in vivo findings reveal that LRRC75A-AS1 promotes breast cancer progression by sponging miR-489-3p and upregulating ARD1. The LRRC75A-AS1/miR-489-3p/ARD1 ceRNA axis represents a novel regulatory pathway and a promising therapeutic target in BC.

miRNA expression also did not correlate with invasiveness (cavernous or sphenoid sinus invasion, optic chiasm compression). Although the total expression of microRNA was significantly lower in NFPAs, hsa-miR-16-5p, hsa-miR-143-3p, and hsa-miR-423-5p are not useful as non-invasive biomarkers in patients with invasive non-functioning pituitary adenomas and prolactinomas.

In this study, we modified MXene with hyaluronic acid (HA) and coloaded it with doxorubicin (DOX) and the nucleic acid miR489 to address chemotherapy resistance by inhibiting DOX efflux and enabling gene interference...Moreover, DTH489 exhibited substantial tumor growth suppression in a mouse model of drug-resistant breast cancer. The results of this research underscore the potential of DTH489 as a multimodal therapeutic platform that effectively reverses chemotherapy resistance in cancer.

These findings suggest that lncRNA-MIR193BHG plays a critical regulatory role in breast cancer bone metastasis, and the lncRNA-MIR193BHG/miR-489-3p/DNMT3A signaling axis could be a potential target for the treatment of breast cancer bone metastasis. Future studies should further explore the broader applicability of this mechanism and its clinical feasibility.

In summary, inhibiting the oncogenic miRNAs and ectopic expression of tumor-suppressive miRNAs can decrease prolactin secretion, reduce tumor invasion and migration, enhance dopamine agonist efficacy, and inhibit prolactinoma development. These findings can serve as a blueprint for future translational studies investigating miR-based therapeutics for prolactinoma.

These findings suggest that miR-489-3p overexpression may inhibit NSCLC cell proliferation and migration by suppressing the HER2/PI3K/AKT/Snail signaling pathway. This study elucidates miR-489-3p's molecular mechanisms in NSCLC and provides experimental basis for identifying early diagnostic markers and novel therapeutic targets.

Additionally, miR-489-3p inhibition partially negated the effects of LINC00115 knockdown in THCA cells, and EVA1A knockdown remarkably impeded the effects of miR-489-3p inhibition in THCA cells. Thus, LINC00115 knockdown suppressed THCA carcinogenesis via targeting miR-489-3p, which regulates EVA1A expression and affects the Hippo signaling pathway.

The TGF-beta and a number of kinase-dependent pathways were also retrieved using the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. This study offers an understanding of the role of AR in TNBC and further implicates miRNAs in mediating the effects of AR on TNBC.

One of the anti-cancer mechanisms through which CMM489 synergizes with PARP inhibitors is the blockade of homologous recombination (HR) in TNBC cells upon DNA damage. The results of this study highlight the potential use of CMM489 in combination treatments with PARP inhibitors in TNBCs.

Pharmacological inhibition of miR-489-3p markedly reversed the effects of Venetoclax-resistant upon AML proliferation and metastasis. Thus, our study suggests that MMP-7 is an essential factor in AML, and regulator the miR-489-3p/MMP7 axis may be a novel treatment strategy for overcoming Venetoclax resistance in AML.

MiR-489-3p inhibition effectively reversed the effects of CRNDE depletion on hypoxia cardiomyocytes (p = 0.0002). These findings offered a promising therapeutic option for the treatment of MI.

The results indicate that knockdown of lncRNA CRNDE ameliorates apoptosis and the inflammatory response in ischemia-reperfusion-induced brain injury through the mir-489-3p/FOXO3 axis. LncRNA CRNDE may represent a novel therapeutic target for brain injury.