ArticlePLoS genetics2023
ARHGAP15 promotes metastatic colonization in gastric cancer by suppressing RAC1-ROS pathway.
Article in PLoS genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Exploring platelet-covered and naked circulating tumor cells - a single-cell transcriptomic perspective.Journal of translational medicine · 2026Article
- Rho GTPases in cancer resistance: mechanisms, vulnerabilities, and therapeutic opportunities.Biochemical Society transactions · 2026Review
- Proteomic atlas of human peritoneal tissue.Scientific reports · 2026Article
- Clonal evolution and stromal crosstalk drive an invasive epithelial program in bladder cancer.Frontiers in cell and developmental biology · 2026Article
- Rac1 in gastric cancer: a molecular driver of invasion, EMT, and therapeutic resistance.Journal of translational medicine · 2025Review
- Oxidative Stress and Redox Signaling in Gastric Cancer: From Mechanisms to Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2025Review
- The mutational landscape and functional effects of noncoding ultraconserved elements in human cancers.Science advances · 2025Article
- Quercetin suppresses ROS production and migration by specifically targeting Rac1 activation in gliomas.Frontiers in pharmacology · 2024Article
- Oxidative Stress, Reductive Stress and Antioxidants in Vascular Pathogenesis and Aging.Antioxidants (Basel, Switzerland) · 2023Review
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Authors and funding
12 authors.
Funding
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Abstract
The molecular mechanism of tumor metastasis, especially how metastatic tumor cells colonize in a distant site, remains poorly understood. Here we reported that ARHGAP15, a Rho GTPase activating protein, enhanced gastric cancer (GC) metastatic colonization, which was quite different from its reported role as a tumor suppressor gene in other cancers. It was upregulated in metastatic lymph nodes and significantly associated with a poor prognosis. Ectopic expression of ARHGAP15 promoted metastatic colonization of gastric cancer cells in murine lungs and lymph nodes in vivo or protected cells from oxidative-related death in vitro. However, genetic downregulation of ARHGAP15 had the opposite effect. Mechanistically, ARHGAP15 inactivated RAC1 and then decreased intracellular accumulation of reactive oxygen species (ROS), thus enhancing the antioxidant capacity of colonizing tumor cells under oxidative stress. This phenotype could be phenocopied by inhibition of RAC1 or rescued by the introduction of constitutively active RAC1 into cells. Taken together, these findings suggested a novel role of ARHGAP15 in promoting gastric cancer metastasis by quenching ROS through inhibiting RAC1 and its potential value for prognosis estimation and targeted therapy.
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