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Research Article

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Mol. Cells 2012; 33(3): 309-316

Published online February 28, 2012

https://doi.org/10.1007/s10059-012-2280-7

© The Korean Society for Molecular and Cellular Biology

Identification of EBP50 as a Specific Biomarker for Carcinogens Via the Analysis of Mouse Lymphoma Cellular Proteome

Yoen Jung Lee, In-Kwon Choi, Yhun Yhong Sheen1, Sue Nie Park2, and Ho Jeong Kwon*

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Department of Biotechnology, Translational Research Center for Protein Function Control, College of Life Science and Biotechnology, Yonsei University, Seoul 120-749, Korea, College of pharmacy, Ewha Womans University, Seoul 120-750, Korea, 2Hazardous Substances Analysis Division at Seoul Regional FDA, Korea Food and Drug Administration, Seoul 158-050, Korea

Correspondence to : *Correspondence: kwonhj@yonsei.ac.kr

Received: December 12, 2011; Revised: January 10, 2012; Accepted: January 11, 2012

Abstract

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To identify specific biomarkers generated upon exposure of L5178Y mouse lymphoma cells to carcinogens, 2-DE and MALDI-TOF MS analysis were conducted using the cellular proteome of L5178Y cells that had been treated with the known carcinogens, 1,2-dibromoethane and O-nitrotoluene and the noncarcinogens, emodin and D-mannitol. Eight protein spots that showed a greater than 1.5-fold increase or decrease in intensity following carci-nogen treatment compared with treatment with noncarci-nogens were selected. Of the identified proteins, we fo-cused on the candidate biomarker ERM-binding phosphoprotein 50 (EBP50), the expression of which was specifically increased in response to treatment with the carcinogens. The expression level of EBP50 was determined by western analysis using polyclonal rabbit anti-EBP50 antibody. Further, the expression level of EBP50 was increased in cells treated with seven additional carcinogens, verifying that EBP50 could serve as a specific biomarker for carcinogens.

Keywords biomarker, carcinogen, EBP50, toxicoproteomics

Article

Research Article

Mol. Cells 2012; 33(3): 309-316

Published online March 31, 2012 https://doi.org/10.1007/s10059-012-2280-7

Copyright © The Korean Society for Molecular and Cellular Biology.

Identification of EBP50 as a Specific Biomarker for Carcinogens Via the Analysis of Mouse Lymphoma Cellular Proteome

Yoen Jung Lee, In-Kwon Choi, Yhun Yhong Sheen1, Sue Nie Park2, and Ho Jeong Kwon*

Department of Biotechnology, Translational Research Center for Protein Function Control, College of Life Science and Biotechnology, Yonsei University, Seoul 120-749, Korea, College of pharmacy, Ewha Womans University, Seoul 120-750, Korea, 2Hazardous Substances Analysis Division at Seoul Regional FDA, Korea Food and Drug Administration, Seoul 158-050, Korea

Correspondence to:*Correspondence: kwonhj@yonsei.ac.kr

Received: December 12, 2011; Revised: January 10, 2012; Accepted: January 11, 2012

Abstract

To identify specific biomarkers generated upon exposure of L5178Y mouse lymphoma cells to carcinogens, 2-DE and MALDI-TOF MS analysis were conducted using the cellular proteome of L5178Y cells that had been treated with the known carcinogens, 1,2-dibromoethane and O-nitrotoluene and the noncarcinogens, emodin and D-mannitol. Eight protein spots that showed a greater than 1.5-fold increase or decrease in intensity following carci-nogen treatment compared with treatment with noncarci-nogens were selected. Of the identified proteins, we fo-cused on the candidate biomarker ERM-binding phosphoprotein 50 (EBP50), the expression of which was specifically increased in response to treatment with the carcinogens. The expression level of EBP50 was determined by western analysis using polyclonal rabbit anti-EBP50 antibody. Further, the expression level of EBP50 was increased in cells treated with seven additional carcinogens, verifying that EBP50 could serve as a specific biomarker for carcinogens.

Keywords: biomarker, carcinogen, EBP50, toxicoproteomics

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.
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