alexa Proteomics Investigation Reveals Apoptosis-Associated Proteins in Aryl Hydrocarbon Receptor-Deficient Human Lung Cells Treated with 2,3,7,8-Tetrachlorobenzo-p-dioxin
ISSN: 0974-276X

Journal of Proteomics & Bioinformatics
Open Access

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Research Article

Proteomics Investigation Reveals Apoptosis-Associated Proteins in Aryl Hydrocarbon Receptor-Deficient Human Lung Cells Treated with 2,3,7,8-Tetrachlorobenzo-p-dioxin

Eric S. L. Hsiao1, Yin-Wei Chang1, Pinpin Lin2* and Pao-Chi Liao1,3,4*

1Department of Environmental and Occupational Health, College of Medicine, National Cheng Kung University, Tainan, Taiwan

2Division of Environmental Health and Occupational Medicine, National Health Research Institutes, Zhunan, Taiwan

3Sustainable Environment Research Center, National Cheng Kung University, Tainan, Taiwan

4Center for Micro/Nano Science and Technology (CMNST), National Cheng Kung University, Tainan, Taiwan

*Corresponding Authors:
Pao-Chi Liao
Department of Environmental Occupational Health
National Cheng Kung University
College of Medicine, 138 Sheng-Li Road
Tainan 70428, Taiwan
Fax: 886-6-2743748
E-mail: [email protected]

Pinpin Lin
Division of Environmental Health and Occupational Medicine
National Health Research Institutes
No. 35 Keyan Road, Zhunan Town
Miaoli County 350, Taiwan
Fax: 886-37-587406 E-mail: [email protected]

Received Date: November 25, 2011; Accepted Date: January 09, 2012; Published Date: January 20, 2012

Citation: Hsiao ESL, Chang YW, Lin P, Liao PC (2012) Proteomics Investigation Reveals Apoptosis-Associated Proteins in Aryl Hydrocarbon Receptor-Deficient Human Lung Cells Treated with 2,3,7,8-Tetrachlorobenzo-p-dioxin. J Proteomics Bioinform 5: 015-023. doi:10.4172/jpb.1000208

Copyright: © 2012 Hsiao ESL, et al. 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 credited.

Abstract

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), the most potent dioxin, binds to aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, which subsequently alters gene expression. Epidemiological studies suggested that exposure to TCDD highly enhanced the risk of pulmonary diseases. In this study, we adopted a comparative proteomic approach using two-dimensional gel electrophoresis (2DE) to identify the differential expression of proteins between TCDD-treated control and AhR-deficient lung adenocarcinoma cells. Fifteen proteins from seventeen differential protein spots were identified that four of which were down-regulated and eleven were up-regulated. Western blotting analysis confirmed differential expression for five identified proteins, including GRB10, YWHAG, HSP27, LGALS1 and ACTB. Further protein-protein interaction network analysis of the identified proteins illustrated that twelve proteins were linked to a network containing caspase-3, p53, MDM2 and Akt/PKB, which is known to be associated with apoptosis pathway. Among the identified proteins, GRB10 may play a critical role to regulate the development of apoptosis in human lung cells by TCDD exposure. According to our study, it is expected to lead to new insights into the apoptosis pathway in lung adenocarcinoma by TCDD exposure.

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