ArticleACS chemical biology2010
A novel and specific NADPH oxidase-1 (Nox1) small-molecule inhibitor blocks the formation of functional invadopodia in human colon cancer cells.
Article in ACS chemical biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed, 185 citations in OpenAlex.
- NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers.Cellular & molecular immunology · 2026Review
- ML-171 Attenuates Pentylenetetrazole-Associated Oxidative and Apoptotic Injury Without Robust Suppression of Seizure Expression: An In Vitro and In Vivo Study.International journal of molecular sciences · 2026Article
- Tryptophan metabolites 3-hydroxykynurenine (3HK) and 3-hydroxyanthranilic acid (3HAA) increase oxidative stress and impair osteoblastic bone formation.The Journal of biological chemistry · 2026Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Review
- NOX Family: Regulators of Reactive Oxygen Species Balance in Tumor Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Painting Cell-Cell Interactions by Horseradish Peroxidase and Endogenously Generated Hydrogen Peroxide.ACS chemical biology · 2025Article
- NOX proteins and ROS generation: role in invadopodia formation and cancer cell invasion.Biological research · 2024Review
- Oxidative Stress Induced by Cortisol in Human Platelets.International journal of molecular sciences · 2024Article
- ROS-mediated thylakoid membrane remodeling and triacylglycerol biosynthesis under nitrogen starvation in the algaFrontiers in plant science · 2024Article
- NOX1 and PRDX6 synergistically support migration and invasiveness of hepatocellular carcinoma cells through enhanced NADPH oxidase activity.Advances in redox research · 2023Article
- Exercise induces superoxide and NOX4 contribution in endothelium-dependent dilation in coronary arterioles from a swine model of chronic myocardial ischemia.Microvascular research · 2023Article
- NADPH Oxidases: From Molecular Mechanisms to Current Inhibitors.Journal of medicinal chemistry · 2023Review
- A predicted structure of NADPH Oxidase 1 identifies key components of ROS generation and strategies for inhibition.PloS one · 2023Article
- NADPH Oxidases in Aortic Aneurysms.Antioxidants (Basel, Switzerland) · 2022Review
- NADPH Oxidases in Pain Processing.Antioxidants (Basel, Switzerland) · 2022Review
- The Mechanisms of Restenosis and Relevance to Next Generation Stent Design.Biomolecules · 2022Review
- NOX1 promotes myocardial fibrosis and cardiac dysfunctionFrontiers in pharmacology · 2022Article
- RND3 attenuates oxidative stress and vascular remodeling in spontaneously hypertensive rat via inhibiting ROCK1 signaling.Redox biology · 2021Article
- The TGF-β/NADPH Oxidases Axis in the Regulation of Liver Cell Biology in Health and Disease.Cells · 2021Review
48 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The NADPH oxidase (Nox) proteins catalyze the regulated formation of reactive oxygen species (ROS), which play key roles as signaling molecules in several physiological and pathophysiological processes. ROS generation by the Nox1 member of the Nox family is necessary for the formation of extracellular matrix (ECM)-degrading, actin-rich cellular structures known as invadopodia. Selective inhibition of Nox isoforms can provide reversible, mechanistic insights into these cellular processes in contrast to scavenging or inhibition of ROS production. Currently no specific Nox inhibitors have been described. Here, by high-throughput screening, we identify a subset of phenothiazines, 2-acetylphenothiazine (here referred to as ML171) (and its related 2-(trifluoromethyl)-phenothiazine) as nanomolar, cell-active, and specific Nox1 inhibitors that potently block Nox1-dependent ROS generation, with only marginal activity on other cellular ROS-producing enzymes and receptors including the other Nox isoforms. ML171 also blocks the ROS-dependent formation of ECM-degrading invadopodia in colon cancer cells. Such effects can be reversed by overexpression of Nox1 protein, which is suggestive of a selective mechanism of inhibition of Nox1 by this compound. These results elucidate the relevance of Nox1-dependent ROS generation in mechanisms of cancer invasion and define ML171 as a useful Nox1 chemical probe and potential therapeutic agent for inhibition of cancer cell invasion.
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