ArticleCellular microbiology2021
Pseudomonas aeruginosa ExoT induces G1 cell cycle arrest in melanoma cells.
Article in Cellular microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
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- The human microbiome: redefining cancer pathogenesis and therapy.Cancer cell international · 2025Review
- Molecular characterization of virulent genes in Pseudomonas aeruginosa based on componential usage divergence.Scientific reports · 2025Article
- Synergy between immune system and antibiotics drives infection control in mice.Frontiers in immunology · 2025Article
- Nanomaterial-assisted oncolytic bacteria in solid tumor diagnosis and therapeutics.Bioengineering & translational medicine · 2024Review
- Role of the gut microbiota in anticancer therapy: from molecular mechanisms to clinical applications.Signal transduction and targeted therapy · 2023Review
- Bacterial-Mediated Tumor Therapy: Old Treatment in a New Context.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Review
- Pseudomonas aeruginosa: pathogenesis, virulence factors, antibiotic resistance, interaction with host, technology advances and emerging therapeutics.Signal transduction and targeted therapy · 2022Review
- CrkII/Abl phosphorylation cascade is critical for NLRC4 inflammasome activity and is blocked by Pseudomonas aeruginosa ExoT.Nature communications · 2022Article
- Article
- DT389-YP7, a Recombinant Immunotoxin against Glypican-3 That Inhibits Hepatocellular Cancer Cells: An In Vitro Study.Toxins · 2021Article
- Therapeutic assessment of N-formyl-methionyl-leucyl-phenylalanine (fMLP) in reducing periprosthetic joint infection.European cells & materials · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Recently, we demonstrated that Pseudomonas aeruginosa Exotoxin T (ExoT) employs two distinct mechanisms to induce potent apoptotic cytotoxicity in a variety of cancer cell lines. We further demonstrated that it can significantly reduce tumour growth in an animal model for melanoma. During these studies, we observed that melanoma cells that were transfected with ExoT failed to undergo mitosis, regardless of whether they eventually succumbed to ExoT-induced apoptosis or survived in ExoT's presence. In this report, we sought to investigate ExoT's antiproliferative activity in melanoma. We delivered ExoT into B16 melanoma cells by bacteria (to show necessity) and by transfection (to show sufficiency). Our data indicate that ExoT exerts a potent antiproliferative function in melanoma cells. We show that ExoT causes cell cycle arrest in G1 interphase in melanoma cells by dampening the G1/S checkpoint proteins. Our data demonstrate that both domains of ExoT; (the ADP-ribosyltransferase (ADPRT) domain and the GTPase activating protein (GAP) domain); contribute to ExoT-induced G1 cell cycle arrest in melanoma. Finally, we show that the ADPRT-induced G1 cell cycle arrest in melanoma cells likely involves the Crk adaptor protein. Our data reveal a novel virulence function for ExoT and further highlight the therapeutic potential of ExoT against cancer.
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Registered trials
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