Overexpression of DBC1, correlated with poor prognosis, is a potential therapeutic target for hepatocellular carcinoma.
Biochem Biophys Res Commun
; 494(3-4): 511-517, 2017 12 16.
Article
em En
| MEDLINE
| ID: mdl-29106957
ABSTRACT
Deleted in Breast Cancer 1 (DBC1) is a regulatory protein involved in cell metabolism and cancer progression. Nevertheless, the expression and prognostic values of DBC1 in hepatocellular carcinoma (HCC) are still not well understood. The following study investigated the clinical significance and biological function of DBC1 in HCC. Briefly, overexpression of DBC1 at transcriptional and translational levels in human HCC tissues compared to adjacent normal tissues was observed using quantitative real-time polymerase chain reaction (qRT-PCR), western blot (WB) and immunohistochemistry (IHC) approach. Furthermore, upregulated DBC1 was significantly correlated with tumor size (p = 0.005), N stage (p = 0.016), M stage (p = 0.011), tumor differentiation (p < 0.001), and American Joint Committee on Cancer (AJCC) stage (p = 0.001). Moreover, Kaplan-Meier survival analysis revealed that DBC1 was an independent prognosis predictor for disease-free survival (DFS) (p < 0.001) and overall survival (OS) (p < 0.001). In addition, by using Cell Counting Kit-8 (CCK8) assays and colony formation assays, we found that the knockdown of DBC1 significantly suppressed the proliferation of HCC cells in vitro. To conclude, these findings demonstrated that DBC1 was essential in tumorigenesis and proliferation. Moreover, it was identified as a potential therapeutic target for HCC.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Biomarcadores Tumorais
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Carcinoma Hepatocelular
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Proteínas Adaptadoras de Transdução de Sinal
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Neoplasias Hepáticas
Tipo de estudo:
Etiology_studies
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Prevalence_studies
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Prognostic_studies
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Risk_factors_studies
Limite:
Aged
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Aged80
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Humans
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Middle aged
País/Região como assunto:
Asia
Idioma:
En
Revista:
Biochem Biophys Res Commun
Ano de publicação:
2017
Tipo de documento:
Article