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Genome-Wide and Differential Proteomic Analysis of Hepatitis B Virus and Aflatoxin B1 Related Hepatocellular Carcinoma in Guangxi, China
Both hepatitis B virus (HBV) and aflatoxin B1 (AFB1) exposure can cause liver damage as well as increase the probability of hepatocellular carcinoma (HCC). To investigate the underlying genetic changes that may influence development of HCC associated with HBV infection and AFB1 exposure, HCC patient...
Autores principales: | , , , , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3877066/ https://www.ncbi.nlm.nih.gov/pubmed/24391771 http://dx.doi.org/10.1371/journal.pone.0083465 |
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author | Qi, Lu-Nan Li, Le-Qun Chen, Yuan-Yuan Chen, Zhao-Hong Bai, Tao Xiang, Bang-De Qin, Xiao Xiao, Kai-Yin Peng, Min-Hao Liu, Zhi-Ming Liu, Tang-Wei Qin, Xue Li, Shan Han, Ze-Guang Mo, Zeng-Nan Santella, Regina M. Winkler, Cheryl A. O’Brien, Stephen J. Peng, Tao |
author_facet | Qi, Lu-Nan Li, Le-Qun Chen, Yuan-Yuan Chen, Zhao-Hong Bai, Tao Xiang, Bang-De Qin, Xiao Xiao, Kai-Yin Peng, Min-Hao Liu, Zhi-Ming Liu, Tang-Wei Qin, Xue Li, Shan Han, Ze-Guang Mo, Zeng-Nan Santella, Regina M. Winkler, Cheryl A. O’Brien, Stephen J. Peng, Tao |
author_sort | Qi, Lu-Nan |
collection | PubMed |
description | Both hepatitis B virus (HBV) and aflatoxin B1 (AFB1) exposure can cause liver damage as well as increase the probability of hepatocellular carcinoma (HCC). To investigate the underlying genetic changes that may influence development of HCC associated with HBV infection and AFB1 exposure, HCC patients were subdivided into 4 groups depending upon HBV and AFB1 exposure status: (HBV(+)/AFB1(+), HBV(+)/AFB1(-), HBV(-)/AFB1(+), HBV(-)/AFB1(-)). Genetic abnormalities and protein expression profiles were analyzed by array-based comparative genomic hybridization and isobaric tagging for quantitation. A total of 573 chromosomal aberrations (CNAs) including 184 increased and 389 decreased were detected in our study population. Twenty-five recurrently altered regions (RARs; chromosomal alterations observed in ≥10 patients) in chromosomes were identified. Loss of 4q13.3-q35.2, 13q12.1-q21.2 and gain of 7q11.2-q35 were observed with a higher frequency in the HBV(+)/AFB1(+), HBV(+)/AFB1(-) and HBV(-)/AFB1(+) groups compared to the HBV(-)/AFB(-) group. Loss of 8p12-p23.2 was associated with high TNM stage tumors (P = 0.038) and was an unfavorable prognostic factor for tumor-free survival (P =0.045). A total of 133 differentially expressed proteins were identified in iTRAQ proteomics analysis, 69 (51.8%) of which mapped within identified RARs. The most common biological processes affected by HBV and AFB1 status in HCC tumorigenesis were detoxification and drug metabolism pathways, antigen processing and anti-apoptosis pathways. Expression of AKR1B10 was increased significantly in the HBV(+)/AFB1(+) and HBV(-)/AFB1(+) groups. A significant correlation between the expression of AKR1B10 mRNA and protein levels as well as AKR1B10 copy number was observered, which suggest that AKR1B10 may play a role in AFB1-related hepatocarcinogenesis. In summary, a number of genetic and gene expression alterations were found to be associated with HBV and AFB1- related HCC. The possible synergistic effects of HBV and AFB1 in hepatocarcinogenesis warrant further investigations. |
format | Online Article Text |
id | pubmed-3877066 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-38770662014-01-03 Genome-Wide and Differential Proteomic Analysis of Hepatitis B Virus and Aflatoxin B1 Related Hepatocellular Carcinoma in Guangxi, China Qi, Lu-Nan Li, Le-Qun Chen, Yuan-Yuan Chen, Zhao-Hong Bai, Tao Xiang, Bang-De Qin, Xiao Xiao, Kai-Yin Peng, Min-Hao Liu, Zhi-Ming Liu, Tang-Wei Qin, Xue Li, Shan Han, Ze-Guang Mo, Zeng-Nan Santella, Regina M. Winkler, Cheryl A. O’Brien, Stephen J. Peng, Tao PLoS One Research Article Both hepatitis B virus (HBV) and aflatoxin B1 (AFB1) exposure can cause liver damage as well as increase the probability of hepatocellular carcinoma (HCC). To investigate the underlying genetic changes that may influence development of HCC associated with HBV infection and AFB1 exposure, HCC patients were subdivided into 4 groups depending upon HBV and AFB1 exposure status: (HBV(+)/AFB1(+), HBV(+)/AFB1(-), HBV(-)/AFB1(+), HBV(-)/AFB1(-)). Genetic abnormalities and protein expression profiles were analyzed by array-based comparative genomic hybridization and isobaric tagging for quantitation. A total of 573 chromosomal aberrations (CNAs) including 184 increased and 389 decreased were detected in our study population. Twenty-five recurrently altered regions (RARs; chromosomal alterations observed in ≥10 patients) in chromosomes were identified. Loss of 4q13.3-q35.2, 13q12.1-q21.2 and gain of 7q11.2-q35 were observed with a higher frequency in the HBV(+)/AFB1(+), HBV(+)/AFB1(-) and HBV(-)/AFB1(+) groups compared to the HBV(-)/AFB(-) group. Loss of 8p12-p23.2 was associated with high TNM stage tumors (P = 0.038) and was an unfavorable prognostic factor for tumor-free survival (P =0.045). A total of 133 differentially expressed proteins were identified in iTRAQ proteomics analysis, 69 (51.8%) of which mapped within identified RARs. The most common biological processes affected by HBV and AFB1 status in HCC tumorigenesis were detoxification and drug metabolism pathways, antigen processing and anti-apoptosis pathways. Expression of AKR1B10 was increased significantly in the HBV(+)/AFB1(+) and HBV(-)/AFB1(+) groups. A significant correlation between the expression of AKR1B10 mRNA and protein levels as well as AKR1B10 copy number was observered, which suggest that AKR1B10 may play a role in AFB1-related hepatocarcinogenesis. In summary, a number of genetic and gene expression alterations were found to be associated with HBV and AFB1- related HCC. The possible synergistic effects of HBV and AFB1 in hepatocarcinogenesis warrant further investigations. Public Library of Science 2013-12-31 /pmc/articles/PMC3877066/ /pubmed/24391771 http://dx.doi.org/10.1371/journal.pone.0083465 Text en © 2013 Qi et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Qi, Lu-Nan Li, Le-Qun Chen, Yuan-Yuan Chen, Zhao-Hong Bai, Tao Xiang, Bang-De Qin, Xiao Xiao, Kai-Yin Peng, Min-Hao Liu, Zhi-Ming Liu, Tang-Wei Qin, Xue Li, Shan Han, Ze-Guang Mo, Zeng-Nan Santella, Regina M. Winkler, Cheryl A. O’Brien, Stephen J. Peng, Tao Genome-Wide and Differential Proteomic Analysis of Hepatitis B Virus and Aflatoxin B1 Related Hepatocellular Carcinoma in Guangxi, China |
title | Genome-Wide and Differential Proteomic Analysis of Hepatitis B Virus and Aflatoxin B1 Related Hepatocellular Carcinoma in Guangxi, China |
title_full | Genome-Wide and Differential Proteomic Analysis of Hepatitis B Virus and Aflatoxin B1 Related Hepatocellular Carcinoma in Guangxi, China |
title_fullStr | Genome-Wide and Differential Proteomic Analysis of Hepatitis B Virus and Aflatoxin B1 Related Hepatocellular Carcinoma in Guangxi, China |
title_full_unstemmed | Genome-Wide and Differential Proteomic Analysis of Hepatitis B Virus and Aflatoxin B1 Related Hepatocellular Carcinoma in Guangxi, China |
title_short | Genome-Wide and Differential Proteomic Analysis of Hepatitis B Virus and Aflatoxin B1 Related Hepatocellular Carcinoma in Guangxi, China |
title_sort | genome-wide and differential proteomic analysis of hepatitis b virus and aflatoxin b1 related hepatocellular carcinoma in guangxi, china |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3877066/ https://www.ncbi.nlm.nih.gov/pubmed/24391771 http://dx.doi.org/10.1371/journal.pone.0083465 |
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