Reactive Oxygen Generated by NADPH Oxidase 1 (Nox1) Contributes to Cell Invasion by Regulating Matrix Metalloprotease-9 Production and Cell Migration

Shirakawa, Masahiro; Adachi, Yoshifumi; Mitsushita, Junji; Kuwabara, Mitsuhiro; Nagasawa, Atsushi; Harada, Saori; Furuta, Shunsuke; Zhang, Yugen; Seheli, Kajla; Miyazaki, Hitoshi; Kamata, Tohru

doi:10.1074/jbc.m109.071779

Cited by 93 publications

(70 citation statements)

References 31 publications

(25 reference statements)

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“…The NF-κB-induced MMP and uPA expressions have also been shown to be regulated by ROS produced from Nox and mitochondria (Nelson and Melendez, 2004;Pelicano et al, 2009;Shinohara et al, 2010;Tobar et al, 2010). Furthermore, the blockade of Nox by diphenyleneiodonium (DPI) abrogates NF-κB activation and inhibits MMP-9 expression, suggesting the role of ROS in NF-κB-induced MMPs expression (Shinohara et al, 2010).…”

Section: Ros and Invasionmentioning

confidence: 99%

Reactive Oxygen Species and Tumor Metastasis

Lee

Kang

2013

Molecules and Cells

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The migration and invasion of cancer cells are the first steps in metastasis. Through a series of cellular responses, including cytoskeletal reorganization and degradation of the extracellular matrix, cancer cells are able to separate from the primary tumor and metastasize to distant locations in the body. In cancer cells, reactive oxygen species (ROS) play important roles in the migration and invasion of cells. Stimulation of cell surface receptors with growth factors and integrin assembly generates ROS, which relay signals from the cell surface to important signaling proteins. ROS then act within cells to promote migration and invasion. In this review, we collect recent evidence pointing towards the involvement of ROS in tumor metastasis and discuss the roles of ROS at different stages during the process of cancer cell migration, invasion and epithelial-mesenchymal transition.

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Section: Ros and Invasionmentioning

confidence: 99%

Reactive Oxygen Species and Tumor Metastasis

Lee

Kang

2013

Molecules and Cells

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“…94 Nox1 also contributes to cell invasion by increasing matrix metalloproteinase (MMP) production ( Figure 6). 95 VEGF-induced blood vessel formation 96 and neovascularization in the ischemic hindlimb 97 are significantly attenuated in Nox2-deficient mice. Thus, Nox2-derived ROS also play an important role in mediating angiogenesis in response to ischemia, although it is not fully understood whether endothelial or monocytic Nox2 primarily contributes to the angiogenic responses.…”

Section: Atherosclerosismentioning

confidence: 99%

Pathophysiological Roles of NADPH Oxidase/Nox Family Proteins in the Vascular System - Review and Perspective -

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Kuroda

Kamouchi

et al. 2011

Circ J

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It has been established that oxidative stress plays a crucial role in the development and progression of vascular diseases. Besides the mitochondria, the NADPH oxidase/Nox family proteins are now thought to be important origins of the reactive oxygen species that underlie various vascular disease states, such as hypertension, atherosclerosis, angiogenesis, and ischemia/reperfusion injury. This review summarizes the basis of vascular Nox proteins and discusses their pathophysiological roles in the vascular system. (Circ J 2011; 75: 1791 - 1800

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“…6A). Importantly, we used significantly lower DPI concentrations (1-100 nM) in our study than the concentrations (10 M) often used for NOX inhibition (25)(26)(27). As we recently showed that infection-dependent ROS production results in caspase-1 activation in epithelial cells (16), we verified that the same DPI concentrations also inhibited caspase-1 activation during chlamydial infection using FLICA Casp1 , a cell-permeable fluorescent reagent that can specifically bind to the active form of caspase-1 (Fig.…”

Section: Nlrx1-mediated Ros Production Is Required For Optimalmentioning

confidence: 99%

Enhancement of Reactive Oxygen Species Production and Chlamydial Infection by the Mitochondrial Nod-like Family Member NLRX1

Abdul-Sater

Saïd-Sadier

Lam

et al. 2010

Journal of Biological Chemistry

125

117

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Chlamydia trachomatis infections cause severe and irreversible damage that can lead to infertility and blindness in both males and females. Following infection of epithelial cells, Chlamydia induces production of reactive oxygen species (ROS). Unconventionally, Chlamydiae use ROS to their advantage by activating caspase-1, which contributes to chlamydial growth. NLRX1, a member of the Nod-like receptor family that translocates to the mitochondria, can augment ROS production from the mitochondria following Shigella flexneri infections. However, in general, ROS can also be produced by membrane-bound NADPH oxidases. Given the importance of ROS-induced caspase-1 activation in growth of the chlamydial vacuole, we investigated the sources of ROS production in epithelial cells following infection with C. trachomatis. In this study, we provide evidence that basal levels of ROS are generated during chlamydial infection by NADPH oxidase, but ROS levels, regardless of their source, are enhanced by an NLRX1-dependent mechanism. Significantly, the presence of NLRX1 is required for optimal chlamydial growth.During electron transfer reactions, eukaryotic cells generate highly reactive O 2 metabolites collectively known as reactive oxygen species (ROS).2 Given their high cellular toxicity, cells have developed mechanisms to maintain the levels of ROS in a homeostatic state and utilize them in cellular functions, including signaling pathways, gene expression regulation, and host defense mechanisms (1-3). Intracellular ROS generation is mediated by several enzymatic reactions, but the bulk of ROS is generated from two sources: the mitochondrial electron transport chain complex and membrane-bound NADPH oxidase (NOX and DUOX) (4).During oxidative phosphorylation in the mitochondria, O 2 is reduced to O 2 . , which in turn is converted by superoxide dismutase into H 2 O 2 , which then diffuses across the mitochondrial membrane to the cytoplasm (4). Notably, NLRX1, a member of the intracellular Nod-like receptor (NLR) family that is localized in mitochondria, enhances ROS production induced by poly(I⅐C), TNF␣, and Shigella flexneri infection (5). Although there is evidence that NLRX1 is the only NLR member that is found in mitochondria, its exact dynamic localization remains to be determined. Results from one study suggested that NLRX1 localizes to the outer mitochondrial membrane (6), but subsequent characterization suggests that NLRX1 is transported to the mitochondrial matrix, where it interacts with UQCRC2, a matrix-facing protein of respiratory chain complex III (bc 1 complex). The bc 1 complex is known to play an essential role in ROS generation from the mitochondria (5, 7). Chlamydia trachomatis is the first cause of bacterial sexually transmitted disease in the United States, and the incidence of infection has been increasing for the past 20 years (8 -10). The bacteria infect their preferred target cells, cervical epithelial cells, through entry vacuoles that avoid fusion with host cell lysosomes and then grow by subverting c...

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Reactive Oxygen Generated by NADPH Oxidase 1 (Nox1) Contributes to Cell Invasion by Regulating Matrix Metalloprotease-9 Production and Cell Migration

Cited by 93 publications

References 31 publications

Reactive Oxygen Species and Tumor Metastasis

Reactive Oxygen Species and Tumor Metastasis

Pathophysiological Roles of NADPH Oxidase/Nox Family Proteins in the Vascular System - Review and Perspective -

Enhancement of Reactive Oxygen Species Production and Chlamydial Infection by the Mitochondrial Nod-like Family Member NLRX1

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