ArticleOncotarget2015
RhoGDI deficiency induces constitutive activation of Rho GTPases and COX-2 pathways in association with breast cancer progression.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- RhoGDI in RBL-2H3 cells acts as a negative regulator of Rho GTPase signaling to inhibit granule exocytosis.Journal of leukocyte biology · 2024Article
- Molecular dynamics simulations reveal the inhibition mechanism of Cdc42 by RhoGDI1.Journal of computer-aided molecular design · 2023Article
- Identifying biomarkers of differential chemotherapy response in TNBC patient-derived xenografts with a CTD/WGCNA approach.iScience · 2023Article
- Correlation between DNA Methylation and Cell Proliferation Identifies New Candidate Predictive Markers in Meningioma.Cancers · 2022Article
- Altered gene expression in human brain microvascular endothelial cells in response to the infection of influenza H1N1 virus.Animal diseases · 2022Article
- Binding of the Andes Virus Nucleocapsid Protein to RhoGDI Induces the Release and Activation of the Permeability Factor RhoA.Journal of virology · 2021Article
- Review
- Molecular subversion of Cdc42 signalling in cancer.Biochemical Society transactions · 2021Review
- Article
- Prognostic Significance of Prostaglandin-Endoperoxide Synthase-2 Expressions in Human Breast Carcinoma: A Multiomic Approach.Cancer informatics · 2020Article
- Tumor-associated factors are enriched in lymphatic exudate compared to plasma in metastatic melanoma patients.The Journal of experimental medicine · 2019Article
- The cytotoxic type 3 secretion system 1 ofScience signaling · 2017Article
- A new role of the Rac-GAP β2-chimaerin in cell adhesion reveals opposite functions in breast cancer initiation and tumor progression.Oncotarget · 2016Article
- Mining for Candidate Genes Related to Pancreatic Cancer Using Protein-Protein Interactions and a Shortest Path Approach.BioMed research international · 2015Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rho GDP Dissociation Inhibitor (RhoGDI) is a key regulator of Rho GTPases. Here we report that loss of RhoGDI significantly accelerated xenograft tumor growth of MDA-MB-231 cells in animal models. At the molecular level, RhoGDI depletion resulted in constitutive activation of Rho GTPases, including RhoA, Cdc42, and Rac1. This was accompanied by Rho GTPase translocation from the cytosol to membrane compartments. Notably, COX-2 protein levels, mRNA expression, and biological activity were markedly increased in RhoGDI-deficient cells. The upregulated expression of COX-2 was directly associated with increased Rho GTPase activity. Further, we assessed the expression level of RhoGDI protein in breast tumor specimens (n = 165) by immunohistochemistry. We found that RhoGDI expression is higher in the early stages of breast cancer followed by a significant decrease in malignant tumors and metastatic lesions (p < 0.01). These data suggest that downregulation of RhoGDI could be a critical mechanism of breast tumor development, which may involve the hyperactivation of Rho GTPases and upregulation of COX-2 activity. Additional studies are warranted to evaluate the therapeutic potential of inhibiting Rho GTPases and COX-2 for treating breast cancers.
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