MiR-141-3p inhibits cell proliferation, migration and invasion by targeting TRAF5 in colorectal cancer.
Biochem Biophys Res Commun
; 514(3): 699-705, 2019 06 30.
Article
em En
| MEDLINE
| ID: mdl-31078266
Emerging evidence has shown that abnormal microRNA (miRNA) expression play an important role in initiation, progression and metastasis in several tumors, including colorectal cancer. Here, we attempted to explore the expression and function of miR-141-3p in colorectal cancer. MiR-141-3p expression was measured in tissue samples, colorectal cancer cell lines and normal human colon epithelium cell line FHC by real-time PCR. The biological roles of miR-141-3p in colorectal cancer were investigated both in vitro and a mouse model in vivo. Bioinformatics analysis, real-time PCR, Western blot and luciferase reporter analysis were performed to validate the association between miR-141-3p and its potential targets. Our results suggested that miR-141-3p expression was down-regulated in colorectal cancer tissues and colorectal cancer cell lines compared to the normal tissues and normal colon cells. Patients with low miR-141-3p had poor outcome. In addition, Overexpression of miR-141-3p significantly delayed the proliferation, migration, and invasion of colorectal cancer cells in vitro, as well as obviously attenuated tumor growth in a xenograft model in vivo. Furthermore, Our results showed that miR-141-3p inhibited the proliferation, migration, and invasion via directly targeting tumor necrosis factor receptor-associated factor 5 (TRAF5). In summary, miR-141-3p acts as a tumor suppressor, via directly targeting TRAF5 and indicated miR-141-3p might be a potential therapeutic target for colorectal cancer.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias Colorretais
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Movimento Celular
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MicroRNAs
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Fator 5 Associado a Receptor de TNF
Tipo de estudo:
Prognostic_studies
Limite:
Animals
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Biochem Biophys Res Commun
Ano de publicação:
2019
Tipo de documento:
Article
País de afiliação:
China