ReviewFrontiers in cell and developmental biology2020
Targeting Rac and Cdc42 GEFs in Metastatic Cancer.
Review in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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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
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Who cites it
76 citing papers in PubMed, 116 citations in OpenAlex.
- Design, green synthesis, and anticancer evaluation of novel sulfaguanidine-based heterocycles as multi-target inhibitors of the VEGFR-2/PI3K/AKT/mTOR pathway.Molecular and cellular biochemistry · 2026Article
- Integrated Cell-Based Transcriptomic and Pathway Profiling Enables Scalable Functional Screening of Bioactive Microalgal Extracts.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Vav2 is a master regulator of repair against bacterial pore-forming toxins.Life science alliance · 2026Article
- How Functional Variants Reconfigure the Rac2 Conformational Landscape.The journal of physical chemistry. B · 2026Article
- The Rho guanine-nucleotide exchange factor P-Rex2 exhibits structural and regulatory features distinct from the related RhoGEF P-Rex1.The Journal of biological chemistry · 2026Article
- FARP1 mediates cMET-driven motility in androgen-independent prostate cancer cells.Endocrinology · 2026Article
- How Functional Variants Reconfigure the Rac2 Conformational Landscape.bioRxiv : the preprint server for biology · 2026Article
- MCM8 promotes colorectal cancer progression by competitively inhibiting HRD1-mediated CDC42 ubiquitination and degradation.Journal of translational medicine · 2026Article
- P-Rex2 exhibits unique structural features and regulatory mechanisms distinct from the closely related RhoGEF P-Rex1.bioRxiv : the preprint server for biology · 2026Article
- DOCK10 Regulates Insulin Hypersecretion in Insulinoma and Serves as a Diagnostic and Therapeutic Target.Cellular and molecular gastroenterology and hepatology · 2026Article
- Decoding Rho GTPase signalling networks in directed cell migration.Frontiers in cell and developmental biology · 2026Review
- New insights into the classification of the RAC1 P29S hotspot mutation in melanoma as an oncogene.Cancer gene therapy · 2025Article
- Up-regulation of NGEF via the BRAFBiochemistry and biophysics reports · 2025Article
- VAV2 Drives EGFR-Mediated Rac1 Responses in Prostate Cancer.Molecular cancer research : MCR · 2025Article
- Deciphering the oncogenic role of Rac family small GTPase 3 in hepatocellular carcinoma through multiomics integration.World journal of hepatology · 2025Article
- CDC42-effector interaction inhibitors alter patterns of vessel arborization in skin and tumorsiScience · 2025Article
- Rho-GTPases subfamily: cellular defectors orchestrating viral infection.Cellular & molecular biology letters · 2025Review
- EGF-Induced Macropinocytosis Promotes NAV1-Dependent Internalization of Occludin in Keratinocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- DNA methylation memory of pancreatic acinar-ductal metaplasia transition state altering Kras-downstream PI3K and Rho GTPase signaling in the absence of Kras mutation.Genome medicine · 2025Article
- Comprehensive computational analysis of differentially expressed miRNAs and their influence on transcriptomic signatures in prostate cancer.Scientific reports · 2025Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The Rho family GTPases Rho, Rac, and Cdc42 have emerged as key players in cancer metastasis, due to their essential roles in regulating cell division and actin cytoskeletal rearrangements; and thus, cell growth, migration/invasion, polarity, and adhesion. This review will focus on the close homologs Rac and Cdc42, which have been established as drivers of metastasis and therapy resistance in multiple cancer types. Rac and Cdc42 are often dysregulated in cancer due to hyperactivation by guanine nucleotide exchange factors (GEFs), belonging to both the diffuse B-cell lymphoma (Dbl) and dedicator of cytokinesis (DOCK) families. Rac/Cdc42 GEFs are activated by a myriad of oncogenic cell surface receptors, such as growth factor receptors, G-protein coupled receptors, cytokine receptors, and integrins; consequently, a number of Rac/Cdc42 GEFs have been implicated in metastatic cancer. Hence, inhibiting GEF-mediated Rac/Cdc42 activation represents a promising strategy for targeted metastatic cancer therapy. Herein, we focus on the role of oncogenic Rac/Cdc42 GEFs and discuss the recent advancements in the development of Rac and Cdc42 GEF-interacting inhibitors as targeted therapy for metastatic cancer, as well as their potential for overcoming cancer therapy resistance.
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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.