Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 1129-1140 |
| Number of pages | 12 |
| Journal | Antioxidants and Redox Signaling |
| Volume | 18 |
| Issue number | 10 |
| DOIs | |
| Publication status | Published - 2013 |
| Externally published | Yes |
Keywords
- dimethylbenz[a]anthracene
- DNA topoisomerase (ATP hydrolysing)
- etoposide
- histone H2AX
- inducible nitric oxide synthase
- nitric oxide
- protein p53
- s nitrosoglutathione
- animal experiment
- article
- carcinogenesis
- controlled study
- cytotoxicity
- DNA cleavage
- DNA sequence
- DNA strand breakage
- enzyme phosphorylation
- inflammation
- macrophage
- melanoma
- mouse
- mutagenesis
- nonhuman
- phenotype
- priority journal
- 9,10-Dimethyl-1,2-benzanthracene
- Animals
- Cell Line
- Cell Transformation, Neoplastic
- Coculture Techniques
- DNA Cleavage
- DNA Topoisomerases, Type II
- Etoposide
- HCT116 Cells
- HL-60 Cells
- Humans
- Inflammation
- Mice
- Mice, Knockout
- Mutagenesis
- Nitric Oxide
- Nitric Oxide Donors
- Pyridines
- S-Nitrosoglutathione
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Topoisomerase II-mediated DNA cleavage and mutagenesis activated by nitric oxide underlie the inflammation-associated tumorigenesis. / Yang, Yu-Chen; Chou, Han-Yi Elizabeth; Shen, Tang-Long; Chang, Wei-Jer; Tai, Pei-Han; Li, Tsai-Kun.
In: Antioxidants and Redox Signaling, Vol. 18, No. 10, 2013, p. 1129-1140.Research output: Contribution to journal › Article › peer-review
}
TY - JOUR
T1 - Topoisomerase II-mediated DNA cleavage and mutagenesis activated by nitric oxide underlie the inflammation-associated tumorigenesis
AU - Yang, Yu-Chen
AU - Chou, Han-Yi Elizabeth
AU - Shen, Tang-Long
AU - Chang, Wei-Jer
AU - Tai, Pei-Han
AU - Li, Tsai-Kun
N1 - 被引用次數：6 Export Date: 7 April 2016 CODEN: ARSIF 通訊地址: Li, T.-K.; Department and Graduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan; 電子郵件： tsaikunli@ntu.edu.tw 化學物質/CAS: dimethylbenz[a]anthracene, 43178-07-0; etoposide, 33419-42-0; inducible nitric oxide synthase, 501433-35-8; nitric oxide, 10102-43-9; s nitrosoglutathione, 57564-91-7; 9,10-Dimethyl-1,2-benzanthracene, 57-97-6; DNA Topoisomerases, Type II, 5.99.1.3; Etoposide, 33419-42-0; Nitric Oxide, 10102-43-9; Nitric Oxide Donors; Pyridines; S-Nitrosoglutathione, 57564-91-7; tris(2-pyridylmethyl)amine 商標： vp 16 參考文獻: Andoh, T., Bis(2,6-dioxopiperazines), catalytic inhibitors of DNA topoisomerase II, as molecular probes, cardioprotectors and antitumor drugs (1998) Biochimie, 80, pp. 235-246; Azarova, A.M., Lyu, Y.L., Lin, C.P., Tsai, Y.C., Lau, J.Y., Wang, J.C., Liu, L.F., Roles of DNA topoisomerase II isozymes in chemotherapy and secondary malignancies (2007) Proc Natl Acad Sci USA, 104, pp. 11014-11019; Bartek, J., Hamerlik, P., Lukas, J., On the origin of prostate fusion oncogenes (2010) Nat Genet, 42, pp. 647-648; Bartkova, J., Horejsi, Z., Koed, K., Kramer, A., Tort, F., Zieger, K., Guldberg, P., Bartek, J., DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis (2005) Nature, 434, pp. 864-870; Calmels, S., Hainaut, P., Ohshima, H., Nitric oxide induces conformational and functional modifications of wild-type p53 tumor suppressor protein (1997) Cancer Res, 57, pp. 3365-3369; Castiglione, N., Rinaldo, S., Giardina, G., Stelitano, V., Cutruzzola, F., Nitrite and nitrite reductases: From molecular mechanisms to significance in human health and disease (2012) Antioxid Redox Signal, 17, pp. 684-716; Chazotte-Aubert, L., Hainaut, P., Ohshima, H., Nitric oxide nitrates tyrosine residues of tumor-suppressor p53 protein in MCF-7 cells (2000) Biochem Biophys Res Commun, 267, pp. 609-613; Chazotte-Aubert, L., Oikawa, S., Gilibert, I., Bianchini, F., Kawanishi, S., Ohshima, H., Cytotoxicity and site-specific DNA damage induced by nitroxyl anion (NO(-)) in the presence of hydrogen peroxide. 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PY - 2013
Y1 - 2013
N2 - Aims: Both cancer-suppressing and cancer-promoting properties of reactive nitrogen and oxygen species (RNOS) have been suggested to play a role in tumor pathology, particularly those activities associated with chronic inflammation. Here, we address the impact of nitric oxide (NO) on the induction of DNA damage and genome instability with a specific focus on the involvement of topoisomerase II (TOP2). We also investigate the contribution of NO to the formation of skin melanoma in mice. Results: Similar to the TOP2-targeting drug, etoposide (VP-16), the NO-donor, S-nitrosoglutathione (GSNO), induces skin melanomas formation in 7,12-dimethyl-benz[a]anthracene (DMBA)-initiated mice. To explore the mechanism(s) underlying this NO-induced tumorigenesis, we use a co-culture model system to demonstrate that inflamed macrophages with inducible NO synthase (iNOS) expression cause γ-H2AX activation, p53 phosphorylation, and chromosome DNA breaks in the target cells. Inhibitor experiments revealed that NO and TOP2 isozymes are responsible for the above described cellular phenotypes. Notably, NO, unlike VP-16, preferentially induces the formation of TOP2β cleavable complexes (TOP2βcc) in cells. Moreover, GSNO induced TOP2-dependent DNA sequence rearrangements and cytotoxicity. Furthermore, the incidences of GSNO-and VP-16-induced skin melanomas were also observed to be lower in the skin-specific top2β-knockout mice. Our results suggest that TOP2 isozymes contribute to NO-induced mutagenesis and subsequent cancer development during chronic inflammation. Innovation and Conclusions: We provide the first experimental evidence for the functional role of TOP2 in NO-caused DNA damage, mutagenesis, and carcinogenesis. Notably, these studies contribute to our molecular understanding of the cancer-promoting actions of RNOS during chronic inflammation. Antioxid. Redox Signal. 18, 1129-1140. © 2013, Mary Ann Liebert, Inc.
AB - Aims: Both cancer-suppressing and cancer-promoting properties of reactive nitrogen and oxygen species (RNOS) have been suggested to play a role in tumor pathology, particularly those activities associated with chronic inflammation. Here, we address the impact of nitric oxide (NO) on the induction of DNA damage and genome instability with a specific focus on the involvement of topoisomerase II (TOP2). We also investigate the contribution of NO to the formation of skin melanoma in mice. Results: Similar to the TOP2-targeting drug, etoposide (VP-16), the NO-donor, S-nitrosoglutathione (GSNO), induces skin melanomas formation in 7,12-dimethyl-benz[a]anthracene (DMBA)-initiated mice. To explore the mechanism(s) underlying this NO-induced tumorigenesis, we use a co-culture model system to demonstrate that inflamed macrophages with inducible NO synthase (iNOS) expression cause γ-H2AX activation, p53 phosphorylation, and chromosome DNA breaks in the target cells. Inhibitor experiments revealed that NO and TOP2 isozymes are responsible for the above described cellular phenotypes. Notably, NO, unlike VP-16, preferentially induces the formation of TOP2β cleavable complexes (TOP2βcc) in cells. Moreover, GSNO induced TOP2-dependent DNA sequence rearrangements and cytotoxicity. Furthermore, the incidences of GSNO-and VP-16-induced skin melanomas were also observed to be lower in the skin-specific top2β-knockout mice. Our results suggest that TOP2 isozymes contribute to NO-induced mutagenesis and subsequent cancer development during chronic inflammation. Innovation and Conclusions: We provide the first experimental evidence for the functional role of TOP2 in NO-caused DNA damage, mutagenesis, and carcinogenesis. Notably, these studies contribute to our molecular understanding of the cancer-promoting actions of RNOS during chronic inflammation. Antioxid. Redox Signal. 18, 1129-1140. © 2013, Mary Ann Liebert, Inc.
KW - dimethylbenz[a]anthracene
KW - DNA topoisomerase (ATP hydrolysing)
KW - etoposide
KW - histone H2AX
KW - inducible nitric oxide synthase
KW - nitric oxide
KW - protein p53
KW - s nitrosoglutathione
KW - animal experiment
KW - article
KW - carcinogenesis
KW - controlled study
KW - cytotoxicity
KW - DNA cleavage
KW - DNA sequence
KW - DNA strand breakage
KW - enzyme phosphorylation
KW - inflammation
KW - macrophage
KW - melanoma
KW - mouse
KW - mutagenesis
KW - nonhuman
KW - phenotype
KW - priority journal
KW - 9,10-Dimethyl-1,2-benzanthracene
KW - Animals
KW - Cell Line
KW - Cell Transformation, Neoplastic
KW - Coculture Techniques
KW - DNA Cleavage
KW - DNA Topoisomerases, Type II
KW - Etoposide
KW - HCT116 Cells
KW - HL-60 Cells
KW - Humans
KW - Inflammation
KW - Mice
KW - Mice, Knockout
KW - Mutagenesis
KW - Nitric Oxide
KW - Nitric Oxide Donors
KW - Pyridines
KW - S-Nitrosoglutathione
U2 - 10.1089/ars.2012.4620
DO - 10.1089/ars.2012.4620
M3 - Article
VL - 18
SP - 1129
EP - 1140
JO - Antioxidants and Redox Signaling
JF - Antioxidants and Redox Signaling
SN - 1523-0864
IS - 10
ER -