MIR582 (MicroRNA 582)

Enrichment results linked the signature to angiogenesis, extracellular matrix remodeling, focal adhesion, and metastasis-associated signatures. These findings support CD81 as a candidate prognostic biomarker and nominate a putative hsa-miR-582-5p-CD81 relationship for future validation.

[This retracts the article DOI: 10.3892/etm.2021.10711.].

Our findings reveal a novel miR-582-3p/PTPRCAP/Wnt/β-catenin axis in LUAD progression, where miR-582-3p drives tumor growth by silencing PTPRCAP and activating Wnt signaling. These results highlight miR-582-3p as a potential therapeutic target and PTPRCAP as a tumor suppressor in LUAD, offering new insights for targeted intervention strategies.

LncRNA NNT-AS1 can serve as a marker of poor prognosis for CRRT treatment as well as participate in AKI by targeting miR-582-5p.

Reconstitution experiments demonstrated that MKRN2 overexpression significantly inhibited tumor cell proliferation, migration/invasion and tumor growth. Our findings establish MKRN2 as a critical regulator of immunosuppressive TME formation through coordinated control of macrophage polarization and NF-κB/COX2 signaling, suggesting its potential as both a prognostic biomarker and therapeutic target for cancer immunotherapy.

PRKCQ-AS1/miR-582-3p axis regulatory relationship exists in lung adenocarcinoma cells. PRKCQ-AS1 may regulate the proliferation, migration and invasion of lung adenocarcinoma cells and participate in LUAD regulation by targeting miR-582-3p.

Down-regulation of DUSP1 expression partially reversed the inhibitory effect of down-regulation of miR-582-5p expression on Mtb-infected macrophages. Conclusion Inhibiting the expression of miR-582-5p can up-regulate DUSP1, thereby inhibiting the proliferation and inflammatory response of Mtb-infected macrophages and promoting cell apoptosis.

In addition, A-H inhibited LUAD proliferation through the miR-582-3p-p27 signaling pathway. These findings may provide a new understanding of the use of Chinese medicine in treating lung cancer.

We therefore developed and successfully tested a novel strategy to discover and deliver miRNAs for glioblastoma and cancer therapy. We developed and used new computational, experimental, and therapeutic approaches to identify and therapeutically deliver master regulatory miRNAs to inhibit the growth of glioblastoma, the most common and deadly primary brain tumor.

The augmented proliferation, migration, and tube formation abilities of cKIF6-overexpressing LECs were attenuated by the inhibitor of cholesterol biosynthesis. The cKIF6 regulates lymphangiogenesis by targeting cholesterol metabolism, making it a promising therapeutic target for lymphangiogenesis-related diseases.