ReviewBiological research2024
NOX proteins and ROS generation: role in invadopodia formation and cancer cell invasion.
Review in Biological research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- Targeting NOX4 with Quercetagetin-PLGA nanomaterials: a novel therapeutic strategy for Alzheimer's disease.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Size-Dependent Differences in the Effects of Low-Dose Selenium Nanoparticles on Chronic Thioacetamide Toxicosis Accompanying HCC Progression in Mice.Biological trace element research · 2026Article
- The prognostic and immunological role of NADPH oxidase in early and locally advanced lung adenocarcinoma.Discover oncology · 2026Article
- Single-Cell sequencing investigation of endoplasmic reticulum stress-related genes in gastric cancer prognostic models and identification of NOX5 as a novel therapeutic target.Translational oncology · 2026Article
- Transcriptional factor ZMYM3 promotes hepatocellular carcinoma metastasis by upregulating CTTN and inducing invadopodia formation.Cell death & disease · 2026Article
- Intercellular mitochondrial transfer in melanoma progression and therapeutic resistance: mechanisms and targeting potential.Frontiers in oncology · 2026Review
- Podosomes and Mechanical Force.Results and problems in cell differentiation · 2026Review
- The Redox Paradox: Cancer's Double-Edged Sword for Malignancy and Therapy.Antioxidants (Basel, Switzerland) · 2025Review
- The Reciprocal Relationship Between Cell Adhesion Molecules and Reactive Oxygen Species.Cells · 2025Review
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
NADPH oxidases (NOX) are membrane-bound proteins involved in the localized generation of reactive oxygen species (ROS) at the cellular surface. In cancer, these highly reactive molecules primarily originate in mitochondria and via NOX, playing a crucial role in regulating fundamental cellular processes such as cell survival, angiogenesis, migration, invasion, and metastasis. The NOX protein family comprises seven members (NOX1-5 and DUOX1-2), each sharing a catalytic domain and an intracellular dehydrogenase site. NOX-derived ROS promote invadopodia formation, aberrant tyrosine kinase activation, and upregulation of matrix metalloproteinases (MMPs). Specifically, NOX5 modulates adhesion, motility, and proteolytic activation, while NOX1 likely contributes to invadopodia formation and adhesive capacity. NOX2 and NOX4 are implicated in regulating the invasive phenotype, expression of MMPs and EMT markers. DUOX1-2 participate in epithelial-mesenchymal transition (EMT), crucial for invasive phenotype development. Soluble molecules such as TGF-β and EGF modulate NOX protein activation, enhancing cell invasion through localized ROS production. This review focuses on elucidating the specific role of NOX proteins in regulating signaling pathways promoting cancer cell spread, particularly EMT, invadopodia formation and invasive capacity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.