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Suppression of tumorigenesis in mitochondrial NADP+-dependent isocitrate dehydrogenase knock-out mice

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Author(s)
Seontae KimSung Youl KimHyeong Jun KuYong Hyun JeonHo Won LeeJaetae LeeTaeg Kyu KwonKwon Moo ParkJeen-Woo Park
Keimyung Author(s)
Kwon, Taeg Kyu
Department
Dept. of Immunology (면역학)
Journal Title
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Issued Date
2014
Volume
1842
Issue
2
Abstract
The tumor host microenvironment is increasingly viewed as an important contributor to tumor growth and suppression. Cellular oxidative stress resulting from high levels of reactive oxygen species (ROS) contributes to various processes involved in the development and progress of malignant tumors including carcinogenesis, aberrant growth, metastasis, and angiogenesis. In this regard, the stroma induces oxidative stress in adjacent tumor cells, and this in turn causes several changes in tumor cells including modulation of the redox status, inhibition of cell proliferation, and induction of apoptotic or necrotic cell death. Because the levels of ROS are determined by a balance between ROS generation and ROS detoxification, disruption of this system will result in increased or decreased ROS level. Recently, we demonstrated that the control of mitochondrial redox balance and cellular defense against oxidative damage is one of the primary functions of mitochondrial NADP+-dependent isocitrate dehydrogenase (IDH2) that supplies NADPH for antioxidant systems. To explore the interactions between tumor cells and the host, we evaluated tumorigenesis between IDH2-deficient (knock-out) and wild-type mice in which B16F10 melanoma cells had been implanted. Suppression of B16F10 cell tumorigenesis was reproducibly observed in the IDH2-deficient mice along with significant elevation of oxidative stress in both the tumor and the stroma. In addition, the expression of angiogenesis markers was significantly down-regulated in both the tumor and the stroma of the IDH2-deficient mice. These results support the hypothesis that redox status-associated changes in the host environment of tumor-bearing mice may contribute to cancer progression.

Keywords
Antioxidant enzyme;
Knockout mice;
Tumorigenesis;
Redox status;
Host microenvironment
Keimyung Author(s)(Kor)
권택규
Publisher
School of Medicine
Citation
Seontae Kim et al. (2014). Suppression of tumorigenesis in mitochondrial NADP+-dependent
isocitrate dehydrogenase knock-out mice. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 1842(2), 135–143. doi: 10.1016/j.bbadis.2013.11.008
Type
Article
ISSN
0925-4439
Source
http://lps3.linkinghub.elsevier.com.proxy.dsmc.or.kr/retrieve/pii/S0925-4439(13)00333-5
DOI
10.1016/j.bbadis.2013.11.008
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/33704
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
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