Knockdown of PNO1 inhibits esophageal cancer progression.
Oncol Rep
; 45(5)2021 05.
Article
em En
| MEDLINE
| ID: mdl-33864661
ABSTRACT
The present study aimed to investigate the role of partner of NOB1 homolog (PNO1) in esophageal cancer (EC). The expression levels of PNO1 in EC were primarily analyzed using data obtained from databases. PNO1 expression was also knocked down in EC cells (Eca109 and TE1) to determine the biological effects of PNO1 on tumorigenesis in vitro and in vivo. In addition, possible downstream targets of PNO1 in EC were identified. The expression levels of PNO1 were upregulated in the tumor tissues compared with that noted in normal tissues. Moreover, the knockdown (KD) of PNO1 suppressed cell proliferation, migration and invasion, and promoted cell apoptosis (P < 0.05). Furthermore, the protein expression levels of AKT1, Twist, Myc, mTOR, matrix metalloproteinase 2 (MMP2), nuclear factor (NF)κB p65 and ßcatenin 1 (CTNNB1) were downregulated following the KD of PNO1 in Eca109 cells (P < 0.05). In addition, the overexpression of CTNNB1 reversed the effects of PNO1 KD in Eca109 cells (P < 0.05). In conclusion, the findings of the present study suggest that PNO1 promotes EC progression by regulating AKT1, Twist, Myc, mTOR, MMP2, NFκB p65 and CTNNB1 expression.
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Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Neoplasias Esofágicas
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Regulação Neoplásica da Expressão Gênica
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Proteínas de Ligação a RNA
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Carcinogênese
Tipo de estudo:
Diagnostic_studies
/
Prognostic_studies
Limite:
Animals
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Female
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Humans
Idioma:
En
Ano de publicação:
2021
Tipo de documento:
Article