MicroRNA-363-3p is downregulated in hepatocellular carcinoma and inhibits tumorigenesis by directly targeting specificity protein 1.
Mol Med Rep
; 16(2): 1603-1611, 2017 Aug.
Article
em En
| MEDLINE
| ID: mdl-28627662
microRNAs exhibit important regulatory roles in tumorigenesis and tumor development, such as in hepatocellular carcinoma (HCC). The present study aimed to investigate the expression and functional roles of microRNA (miR)3633p in HCC. miR-363-3p expression levels in a number of HCC tissues and cell lines were measured by reverse transcription-quantitative PCR (RTqPCR). The effects of miR3633p expression on HCC cell proliferation, migration and invasion were exa-mined by MTT assay, Transwell migration and invasion assay, respectively. The effects of miR3633p on its downstream target gene, specificity protein 1 (SP1), were examined by bioinformatics analysis, luciferase reporter assay, RTqPCR and western blotting. An SP1 overexpression vector was subsequently transfected into HCC cells to assess any selective effects on miR3633p in modulating HCC. The results revealed that miR3633p expression levels were downregulated in both HCC tissues and cell lines, and this low expression level was correlated with tumor size, tumornodemetastasis stage and venous infiltration in patients with HCC. Upregulation of miR3633p inhibited cell proliferation, migration and invasion in HCC cell cultures. In HCC cells transfected with an SP1 expression vector the miR3633pinduced tumor suppressive roles on cell proliferation, migration and invasion were reversed. In conclusion, results from the present study indicated that miR3633p is a tumor suppressor in HCC and functions through a mechanism involving SP1, suggesting that miR3633p may be a potential new therapeutic target for the treatment of HCC.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fator de Transcrição Sp1
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Carcinoma Hepatocelular
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MicroRNAs
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Carcinogênese
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Neoplasias Hepáticas
Limite:
Female
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Humans
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Male
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Middle aged
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article