Prostate cancer invasion is promoted by the miR-96-5p-induced NDRG1 deficiency through NF-κB regulation
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
38697817
DOI
10.48095/ccko202495
PII: 137191
Knihovny.cz E-zdroje
- Klíčová slova
- EMT, NDRG1, NF- kB, miR-96-5p, prostate cancer,
- MeSH
- epitelo-mezenchymální tranzice MeSH
- intracelulární signální peptidy a proteiny * genetika metabolismus MeSH
- invazivní růst nádoru * MeSH
- lidé MeSH
- mikro RNA * genetika MeSH
- myši MeSH
- nádorové buněčné linie MeSH
- nádory prostaty * patologie genetika metabolismus MeSH
- NF-kappa B * metabolismus MeSH
- pohyb buněk MeSH
- proteiny buněčného cyklu * genetika metabolismus MeSH
- regulace genové exprese u nádorů MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- intracelulární signální peptidy a proteiny * MeSH
- mikro RNA * MeSH
- MIRN96 microRNA, human MeSH Prohlížeč
- N-myc downstream-regulated gene 1 protein MeSH Prohlížeč
- NF-kappa B * MeSH
- proteiny buněčného cyklu * 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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