miR-184 expression

This study underscores the pivotal role of the circ-ITCH/miR-184/FOXO3 axis in regulating BCa cell proliferation and migration. It introduces a potential therapeutic target for bladder cancer, suggesting that strategies like circ-ITCH overexpression and miR-184 inhibition could offer promising treatment options.

Our data indicated that miR-184 expression is increased in myeloma plasma cells. Down-regulation of miR-184 promotes MM cell apoptosis and inhibits proliferation and colony formation by regulating Notch1 expression.

Our study revealed that hnRNPA2B1-mediated exosomal transfer of tumor-suppressive miR-184-3p from breast cancer cells to macrophages was an important mediator of TNBCs progression, providing new insights into TNBCs pathogenesis and therapeutic strategies.

MiR-184 repressed LUAD cell processes via mediating C1QTNF6. MiR-184 and C1QTNF6 are expected to be indicators for LUAD treatment.

The expression of miR-184 in serum exosomes of the 33 surviving patients is significantly lower than that of the nonsurviving group (p < 0.05). The expression level of miR-184 in serum exosomes of NSCLC patients is significantly increased, which has a certain value for the differential diagnosis of the nature of benign and malignant lung diseases and is closely related to the prognosis of patients.

The inhibitory effect of miR-184 mimic on cell behaviors was reversed by upregulation of DLX1. These findings suggest that miR-184 plays a beneficial role in suppressing the tumorigenesis of PC by directly targeting DLX1, and it may represent a potential therapeutic strategy for PC.

This research suggested that by interacting with miR-184, tripterine could restrain the progression of BC. This knowledge could be instrumental in developing highly effective treatment solutions for BC.