Knockdown of lncRNA PVT1 inhibits the proliferation and accelerates the apoptosis of colorectal cancer cells via the miR761/MAPK1 axis.
Mol Med Rep
; 24(5)2021 11.
Article
em En
| MEDLINE
| ID: mdl-34515320
ABSTRACT
Colorectal cancer (CRC) is associated with high morbidity rates. Long noncoding RNAs (lncRNAs) participate in the development of CRC. However, the potential roles of lncRNA plasmacytoma variant translocation 1 (PVT1) in CRC remain unknown. Therefore, the aim of the present study was to investigate the potential roles of PVT1 in CRC. Reverse transcriptionquantitative PCR and western blot analyses were conducted to determine the mRNA and protein expression levels. The cellular behaviors were detected using 5Ethynyl2'deoxyuridine, Cell Counting Kit8 and flow cytometry assays. The interaction between PVT1 and microRNA (miR)761 or MAPK1 was confirmed using a dualluciferase reporter assay. Moreover, the Pearson's method was applied for correlation analysis. The results demonstrated that the expression levels of PVT1 and MAPK1 were upregulated, while miR761 was downregulated in CRC tissues. The expression of PVT1 was positively correlated with MAPK1 and negatively correlated with miR761. In addition, PVT1 sponged miR761 to upregulate MAPK1 expression. It was found that the knockdown of PVT1 expression inhibited the proliferation and promoted the apoptosis of CRC cells, which was more potent in cells transfected with miR761. The regulatory role of small interfering RNAPVT1 on the expression of apoptosisrelated genes was reduced by MAPK1. Collectively, the present results suggested that knockdown of PVT1 may inhibit the progression of CRC by regulating the miR761/MAPK1 axis, which may provide a promising biomarker for the treatment of CRC.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias Colorretais
/
MicroRNAs
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RNA Longo não Codificante
Limite:
Humans
País/Região como assunto:
Asia
Idioma:
En
Revista:
Mol Med Rep
Ano de publicação:
2021
Tipo de documento:
Article