Constitutive NF-kappa B activation and tumor-growth promotion by Romo1-mediated reactive oxygen species production
- Authors
- Chung, Jin Sil; Lee, Sora; Yoo, Young Do
- Issue Date
- 8-8월-2014
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Reactive oxygen species; Nuclear factor-kappa B; Tumor growth; Hepatocellular carcinoma; Romo1; Oxidative stress
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.450, no.4, pp.1656 - 1661
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 450
- Number
- 4
- Start Page
- 1656
- End Page
- 1661
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/97701
- DOI
- 10.1016/j.bbrc.2014.07.059
- ISSN
- 0006-291X
- Abstract
- Deregulation of nuclear factor-kappa B (NF-kappa B) and related pathways contribute to tumor cell proliferation and invasion. Mechanisms for constitutive NF-kappa B activation are not fully explained; however, the underlying defects appear to generate and maintain pro-oxidative conditions. In hepatocellular carcinoma (HCC) tissues, up-regulation of reactive oxygen species modulator 1 (Romo1) correlates positively with tumor size. In the present study, we showed that Romo1 expression is required to maintain constitutive nuclear DNA-binding activity of NF-kappa B and transcriptional activity through constitutive I kappa B alpha phosphorylation. Overexpression of Romo1 promoted p65 nuclear translocation and DNA-binding activity. We also show that Romo1 depletion suppressed anchorage-independent colony formation by HCC cells and suppressed tumor growth in vivo. Based on these findings, Romo1 may be a principal regulatory factor in the maintenance of constitutive NF-kappa B activation in tumor cells. In the interest of anti-proliferative treatments for cancer, Romo1 may also present a productive target for drug development. (C) 2014 Elsevier Inc. All rights reserved.
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