Pairedrelated homeobox 1 overexpression promotes multidrug resistance via PTEN/PI3K/AKT signaling in MCF7 breast cancer cells.
Mol Med Rep
; 22(4): 3183-3190, 2020 Oct.
Article
em En
| MEDLINE
| ID: mdl-32945446
ABSTRACT
Multidrug resistance (MDR) is a major cause of disease relapse and mortality in breast cancer. Pairedrelated homeobox 1 (PRRX1) is associated with the epithelialmesenchymal transition (EMT), which is involved in tumor development, including cell invasion and MDR. However, the effect of PRRX1 on MDR had not clearly established. The present study investigated the influence of PRRX1 on MDR and the underlying molecular mechanisms in MCF7 breast cancer cells. MCF7 cells were divided into PRRX1+ group (cells transfected with a recombinant plasmid carrying the PRRX1 gene), negative control group (cells transfected with a blank vector) and blank group (untreated cells). It was found that the relative protein and mRNA expression levels of PRRX1, Ncadherin, vimentin and Pglycoprotein were significantly higher in PRRX1overexpressing MCF7 cells compared with those in control cells. The halfmaximal inhibitory concentration of three groups after treatment with docetaxel and cisplatinum complexes were significantly higher in PRRX1overexpressing MCF7 cells compared with those in control cells. Furthermore, relative PTEN expression decreased significantly and levels of phosphorylated PI3K and AKT increased substantially in PRRX1overexpressing MCF7 cells. These results indicated that PRRX1 overexpression may induce MDR via PTEN/PI3K/AKT signaling in breast cancer. It is highly recommended that PRRX1 gene expression detection should be performed in patients with breast cancer to aid the selection of more appropriate treatments, which will lead to an improved prognosis in clinical practice.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias da Mama
/
Proteínas de Homeodomínio
/
Resistência a Múltiplos Medicamentos
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Resistencia a Medicamentos Antineoplásicos
Limite:
Female
/
Humans
Idioma:
En
Revista:
Mol Med Rep
Ano de publicação:
2020
Tipo de documento:
Article