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Mol. Cells 2010; 30(5): 485-491

Published online September 16, 2010

https://doi.org/10.1007/s10059-010-0136-6

© The Korean Society for Molecular and Cellular Biology

Systems-Level Analysis of Gene Expression Data Revealed NR0B2/SHP as Potential Tumor Suppressor in Human Liver Cancer

Yun-Yong Park*, Hueng-Sik Choi1, and Ju-Seog Lee

Department of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77054, USA, 1Hormone Research Center, School of Biological Sciences and Technology, Chonnam National University, Gwangju 500-757, Korea

Correspondence to : *Correspondence: yypark@mdanderson.org

Received: May 14, 2010; Revised: August 2, 2010; Accepted: August 24, 2010

Abstract

Nuclear receptors (NRs) play pivotal roles in cell growth, proliferation, differentiation and homeostasis. Recent progress demonstrates that NR is tightly linked to human disease such as cancer, diabetes and obesity. Here we explore NR expression profiles in human tissue using systematic approaches. NR gene profiles reveal that individual NR has its own gene expression signature depending on tissue type. Of many organs, NRs expression is enriched in liver. Expression of many NRs was significantly changed in liver cancer. Notably, NR0B2/SHP expression level was significantly decreased in human liver cancer but not in normal liver. In addition, expression of SHP is well associated with good prognosis. SHP gene network analysis based on microarray data in liver cancer shows that SHP regulates cell proliferation and metabolism related gene sets. Our systematic approaches suggest that loss of SHP expression in liver might be key genetic events during hepatocarcinogenesis.

Keywords gene expression, gene signature, human cancer, nuclear receptor

Article

Communication

Mol. Cells 2010; 30(5): 485-491

Published online November 30, 2010 https://doi.org/10.1007/s10059-010-0136-6

Copyright © The Korean Society for Molecular and Cellular Biology.

Systems-Level Analysis of Gene Expression Data Revealed NR0B2/SHP as Potential Tumor Suppressor in Human Liver Cancer

Yun-Yong Park*, Hueng-Sik Choi1, and Ju-Seog Lee

Department of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77054, USA, 1Hormone Research Center, School of Biological Sciences and Technology, Chonnam National University, Gwangju 500-757, Korea

Correspondence to:*Correspondence: yypark@mdanderson.org

Received: May 14, 2010; Revised: August 2, 2010; Accepted: August 24, 2010

Abstract

Nuclear receptors (NRs) play pivotal roles in cell growth, proliferation, differentiation and homeostasis. Recent progress demonstrates that NR is tightly linked to human disease such as cancer, diabetes and obesity. Here we explore NR expression profiles in human tissue using systematic approaches. NR gene profiles reveal that individual NR has its own gene expression signature depending on tissue type. Of many organs, NRs expression is enriched in liver. Expression of many NRs was significantly changed in liver cancer. Notably, NR0B2/SHP expression level was significantly decreased in human liver cancer but not in normal liver. In addition, expression of SHP is well associated with good prognosis. SHP gene network analysis based on microarray data in liver cancer shows that SHP regulates cell proliferation and metabolism related gene sets. Our systematic approaches suggest that loss of SHP expression in liver might be key genetic events during hepatocarcinogenesis.

Keywords: gene expression, gene signature, human cancer, nuclear receptor

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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