Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0019204 (
hepatocellular carcinoma
)
71,386
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
N-acetyltransferase 10
(
NAT10
) is a nucleolar protein involved in histone acetylation, telomerase activity regulation, DNA damage response and cytokinesis. The expression of
NAT10
was found to be enhanced in several types of tumors, suggesting its correlation with tumor development. However, the specific role of
NAT10
in
hepatocellular carcinoma
(
HCC
) is still unclear. The aim of this study was to investigate the expression of
NAT10
in
HCC
patients and to assess the relationship of
NAT10
expression with clinicopathological characteristics and tumor prognosis. We selected 17 pairs of
HCC
samples and adjacent non-neoplastic tissue for mRNA expression analysis. We also performed immunohistochemistry in 186
HCC
samples to evaluate the NAT10 protein expression. Cox regression and Kaplan-Meier analysis was used to study the diagnostic and prognostic value of
NAT10
. The results showed that
NAT10
expression was mainly localized in the nuclei/nucleoli and was significantly higher in
HCC
tissues than peritumoral tissues (P < 0.01). High
NAT10
expression was positively correlated with histological differentiation (P < 0.01) and TNM classification (P < 0.01). Cox regression univariate and multivariable analysis revealed that expression of
NAT10
in
HCC
was an independent prognostic factor for patient survival time. Our data suggested that
NAT10
might be a promising prognostic marker and potential therapeutic target in
HCC
.
...
PMID:High expression of N-acetyltransferase 10: a novel independent prognostic marker of worse outcome in patients with hepatocellular carcinoma. 2682 2
Dysregulation of
N-acetyltransferase 10
(
NAT10
) is associated with the development of many types of tumors; however, its role in
hepatocellular carcinoma
(
HCC
) has not been fully elucidated. Here, we examined the role of
NAT10
during epithelial-to-mesenchymal transition (EMT) in
HCC
and established its role in metastasis. We evaluated expression of
NAT10
expression in four
HCC
cell lines and determined the effects of knockdown by siRNA or treatment with the
NAT10
inhibitor, Remodelin.
NAT10
was highly expressed in
HCC
cell lines with a mesenchymal-like phenotype (SNU387 and SNU449). Knockdown or inhibition of
NAT10
resulted in diminished cell invasion and migration. Moreover, decreased levels of
NAT10
were correlated with increased E-cadherin expression and down regulation of vimentin, both of which are canonical markers of EMT signaling, suggesting that
NAT10
-promoted metastasis may be mediated by EMT in
HCC
. Our data suggests that up regulation of
NAT10
-promoted metastasis of
HCC
cells may be mediated by EMT.
...
PMID:Up regulation of NAT10 promotes metastasis of hepatocellular carcinoma cells through epithelial-to-mesenchymal transition. 2783 5
