Prostate cancer invasion is promoted by the miR-96-5p-induced NDRG1 deficiency through NF-κB regulation
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
38697817
DOI
10.48095/ccko202495
PII: 137191
Knihovny.cz E-resources
- Keywords
- EMT, NDRG1, NF- kB, miR-96-5p, prostate cancer,
- MeSH
- Epithelial-Mesenchymal Transition MeSH
- Intracellular Signaling Peptides and Proteins * genetics metabolism MeSH
- Neoplasm Invasiveness * MeSH
- Humans MeSH
- MicroRNAs * genetics MeSH
- Mice MeSH
- Cell Line, Tumor MeSH
- Prostatic Neoplasms * pathology genetics metabolism MeSH
- NF-kappa B * metabolism MeSH
- Cell Movement MeSH
- Cell Cycle Proteins * genetics metabolism MeSH
- Gene Expression Regulation, Neoplastic MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Intracellular Signaling Peptides and Proteins * MeSH
- MicroRNAs * MeSH
- MIRN96 microRNA, human MeSH Browser
- N-myc downstream-regulated gene 1 protein MeSH Browser
- NF-kappa B * MeSH
- Cell Cycle Proteins * MeSH
BACKGROUND: The N-myc downstream-regulated gene 1 (NDRG1) has been discovered as a significant gene in the progression of cancers. However, the regulatory mechanism of NDRG1 remained obscure in prostate cancer (PCa). METHODS: The miR-96-5p and NDRG1 expression levels were evaluated in PCa cell lines, and prostate tissues, and validated in public databases by real-time polymerase chain reaction, western blot analysis, and immunohistochemistry. The function of miR-96-5p and NDRG1 were investigated by scratch assay and transwell assays in vitro, and mouse xenograft assay in vivo. The candidate pathway regulated by NDRG1 was conducted by the next-generation gene sequencing technique. Immunofluorescence and luciferase assays were used to detect the relation between miR-96-5p, NDRG1, and NF-kB pathway. RESULTS: Overexpressing NDRG1 suppresses the migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro, and inhibits metastasis in vivo. Moreover, miR-96-5p contributes to NDRG1 deficiency and promotes PCa cell migration and invasion. Furthermore, NDRG1 loss activates the NF-kB pathway, which stimulates p65 and IKBa phosphorylation and induces EMT in PCa. CONCLUSIONS: MiR-96-5p promotes the migration and invasion of PCa by targeting NDRG1 and regulating the NF-kB pathway.
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