Clinical Value and Regulatory Mechanism of miR-767-5p in Colorectal Cancer
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
40308200
DOI
10.14712/fb2025071010018
PII: fb_2025071010018
Knihovny.cz E-zdroje
- Klíčová slova
- NFIA, colorectal cancer, interaction, miR-767-5p,
- MeSH
- invazivní růst nádoru MeSH
- Kaplanův-Meierův odhad MeSH
- kolorektální nádory * genetika patologie metabolismus MeSH
- lidé středního věku MeSH
- lidé MeSH
- mikro RNA * genetika metabolismus MeSH
- nádorové buněčné linie MeSH
- pohyb buněk genetika MeSH
- prognóza MeSH
- proliferace buněk genetika MeSH
- regulace genové exprese u nádorů * MeSH
- senioři MeSH
- transkripční faktory NFI metabolismus genetika MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- mikro RNA * MeSH
- transkripční faktory NFI MeSH
The poor prognosis of colorectal cancer (CRC) contributes to a yearly increase in CRC mortality, while microRNAs (miRNAs) were found to play a regulatory function in diversiform cancers, including CRC. The objective of this research was to evaluate the clinical value and possible regulatory mechanisms of miR-767-5p in CRC. The expression level of miR-767-5p in CRC tissues and cells was examined. The Kaplan-Meier curve was utilized to analyse the function of miR-767-5p in CRC prognosis. The independent prognostic factors in CRC were assessed by a multivariate COX regression analysis. Additionally, the regulatory mechanism of miR-767-5p in CRC was determined through an in vitro cell experiment. The miR-767-5p expression was down-regulated in CRC tumour tissues and CRC cells. Indicators such as tumour differentiation, TNM, LNM and miR-767-5p were identified as independent prognostic factors for a poor CRC prognosis. The regulatory relationship between miR-767-5p and nuclear factor I A (NFIA) was verified by the dual-luciferase reporter assay, and the NFIA expression level was significantly suppressed by over-expressed miR-767-5p. The proliferation, migration and invasion of CRC cells were inhibited by over-expressing miR-767-5p, while the inhibition effect could be reversed by over-expressing NFIA. The over-expressed miR-767-5p could serve as a tumour suppressor to inhibit the progression of CRC by suppressing the expression level of NFIA.
Department of Oncology No 971 Navy Hospital of the Chinese People's Liberation Army Qingdao China
Department of Pathology Affiliated Hospital of Hebei University Baoding China
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