MIR4465 (MicroRNA 4465)

Our study demonstrates that Emodin induces ferroptosis through the miR-4465/NFE2L3/HMGCR/GPX4 axis in HCC, revealing NFE2L3's role in ferroptosis and suggesting Emodin as a promising therapeutic candidate.

In addition, CN-3 could upregulate the expression of miR-4465 in cells, thereby inhibiting migration and invasion of glioma cells. These results elucidate the mechanism by which CN-3, a steroidal saponin from the sea, may inhibit the invasive behavior of glioma cells through the miRNA-4465/HMGA1/NF-κB pathway, which also raise the prospect of using CN-3 as a chemotherapeutic agent to prevent glioma invasive growth.

Inhibition of miR-4465 mitigated the role of silenced THUMPD3-AS1 in HCC. This study stresses that THUMPD3-AS1 induces EMT in HCC cells and ultimately promotes HCC cell growth and migration by competitively inhibiting miR-4465 expression and thus upregulating KPNA2.

In conclusion, miR-4465 regulates GSK-3β expression but does not consistently affect RCC cell function as a single molecule. Further comprehensive investigation of regulatory networks is required in this field.

The combined detection of miR-106b-5p, miR-93-5p, miR-3129-5p, miR-199b-3p, miR-4465, and OLR1 is expected to become a molecular biomarker for the long-term prognostic assessment of ovarian cancer.

We conclude that hypoxia upregulates miR-4465 and miR-616-3p expression in PSC-derived exosomes. Following exosome uptake, these miRNAs promote PC progression and metastasis by suppressing the PTEN/AKT pathway.