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BCAT1 promotes tumor cell migration and invasion in hepatocellular carcinoma

Branched-chain amino acid transaminase 1 (BCAT1) has been associated with numerous types of tumors; however, few previous studies have evaluated the expression and role of BCAT1 in hepatocellular carcinoma (HCC). In the present study, the expression of BCAT1 was detected by reverse transcription-qua...

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Autores principales: Xu, Meng, Liu, Qingquan, Jia, Yuli, Tu, Kangsheng, Yao, Yingmin, Liu, Qingguang, Guo, Cheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5038498/
https://www.ncbi.nlm.nih.gov/pubmed/27698837
http://dx.doi.org/10.3892/ol.2016.4969
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author Xu, Meng
Liu, Qingquan
Jia, Yuli
Tu, Kangsheng
Yao, Yingmin
Liu, Qingguang
Guo, Cheng
author_facet Xu, Meng
Liu, Qingquan
Jia, Yuli
Tu, Kangsheng
Yao, Yingmin
Liu, Qingguang
Guo, Cheng
author_sort Xu, Meng
collection PubMed
description Branched-chain amino acid transaminase 1 (BCAT1) has been associated with numerous types of tumors; however, few previous studies have evaluated the expression and role of BCAT1 in hepatocellular carcinoma (HCC). In the present study, the expression of BCAT1 was detected by reverse transcription-quantitative polymerase chain reaction and immunoblotting in six HCC cell lines and 74 pairs of HCC and adjacent non-cancerous liver tissues. In addition, the correlation between the expression levels of c-Myc and BCAT1 was analyzed using immunohistochemistry. Furthermore, RNA silencing was performed using c-Myc-specific or BCAT1-specific small interfering RNA, after which wound healing and Transwell cell invasion assays were performed. Finally, the clinicopathological characteristics of BCAT1 in patients with HCC were analyzed. It was shown that the expression of BCAT1 was significantly higher in HCC tissues compared with adjacent non-tumor tissues (P<0.001), and in HCC cell lines compared within the L-02 hepatic cell line (P<0.001). In addition, immunohistochemical analyses indicated that the expression of BCAT1 was positively correlated with c-Myc (r=0.706, P<0.001). BCAT1 expression was shown to be downregulated in c-Myc-knockdown cells, and silencing of BCAT1 expression reduced the invasion and migration of HCC cells. Furthermore, a clinical analysis indicated that BCAT1 expression in HCC tissues was significantly associated with the tumor-node-metastasis stage, tumor number and tumor differentiation (all P<0.05), and that BCAT1 was able to predict the 5-year survival and disease-free survival rates of patients with HCC (both P<0.001). The results of the present study suggested that BCAT1 expression is upregulated in patients with HCC, and that BCAT1 may serve as a potential molecular target for the diagnosis and treatment of HCC.
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spelling pubmed-50384982016-10-03 BCAT1 promotes tumor cell migration and invasion in hepatocellular carcinoma Xu, Meng Liu, Qingquan Jia, Yuli Tu, Kangsheng Yao, Yingmin Liu, Qingguang Guo, Cheng Oncol Lett Articles Branched-chain amino acid transaminase 1 (BCAT1) has been associated with numerous types of tumors; however, few previous studies have evaluated the expression and role of BCAT1 in hepatocellular carcinoma (HCC). In the present study, the expression of BCAT1 was detected by reverse transcription-quantitative polymerase chain reaction and immunoblotting in six HCC cell lines and 74 pairs of HCC and adjacent non-cancerous liver tissues. In addition, the correlation between the expression levels of c-Myc and BCAT1 was analyzed using immunohistochemistry. Furthermore, RNA silencing was performed using c-Myc-specific or BCAT1-specific small interfering RNA, after which wound healing and Transwell cell invasion assays were performed. Finally, the clinicopathological characteristics of BCAT1 in patients with HCC were analyzed. It was shown that the expression of BCAT1 was significantly higher in HCC tissues compared with adjacent non-tumor tissues (P<0.001), and in HCC cell lines compared within the L-02 hepatic cell line (P<0.001). In addition, immunohistochemical analyses indicated that the expression of BCAT1 was positively correlated with c-Myc (r=0.706, P<0.001). BCAT1 expression was shown to be downregulated in c-Myc-knockdown cells, and silencing of BCAT1 expression reduced the invasion and migration of HCC cells. Furthermore, a clinical analysis indicated that BCAT1 expression in HCC tissues was significantly associated with the tumor-node-metastasis stage, tumor number and tumor differentiation (all P<0.05), and that BCAT1 was able to predict the 5-year survival and disease-free survival rates of patients with HCC (both P<0.001). The results of the present study suggested that BCAT1 expression is upregulated in patients with HCC, and that BCAT1 may serve as a potential molecular target for the diagnosis and treatment of HCC. D.A. Spandidos 2016-10 2016-08-08 /pmc/articles/PMC5038498/ /pubmed/27698837 http://dx.doi.org/10.3892/ol.2016.4969 Text en Copyright: © Xu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Xu, Meng
Liu, Qingquan
Jia, Yuli
Tu, Kangsheng
Yao, Yingmin
Liu, Qingguang
Guo, Cheng
BCAT1 promotes tumor cell migration and invasion in hepatocellular carcinoma
title BCAT1 promotes tumor cell migration and invasion in hepatocellular carcinoma
title_full BCAT1 promotes tumor cell migration and invasion in hepatocellular carcinoma
title_fullStr BCAT1 promotes tumor cell migration and invasion in hepatocellular carcinoma
title_full_unstemmed BCAT1 promotes tumor cell migration and invasion in hepatocellular carcinoma
title_short BCAT1 promotes tumor cell migration and invasion in hepatocellular carcinoma
title_sort bcat1 promotes tumor cell migration and invasion in hepatocellular carcinoma
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5038498/
https://www.ncbi.nlm.nih.gov/pubmed/27698837
http://dx.doi.org/10.3892/ol.2016.4969
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