ArticleCancer research2014
CDC42 inhibition suppresses progression of incipient intestinal tumors.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 56 citations in OpenAlex.
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- Genetic attenuation of ALDH1A1 increases metastatic potential and aggressiveness in colorectal cancer.Molecular oncology · 2026Article
- Rho GTPases in cancer resistance: mechanisms, vulnerabilities, and therapeutic opportunities.Biochemical Society transactions · 2026Review
- β2-Chimaerin Deficiency Favors Polyp Growth in the Colon of ApcMolecules (Basel, Switzerland) · 2025Article
- Exploring the Molecular Targets and Therapeutic Potential of Coptisine in Colon Cancer: A Network Pharmacology Approach.Current medicinal chemistry · 2025Article
- PLGA-PEG Nanoparticles Loaded with Cdc42 Inhibitor for Colorectal Cancer Targeted Therapy.Pharmaceutics · 2024Article
- Ion Transport Basis of Diarrhea, Paneth Cell Metaplasia, and Upregulation of Mechanosensory Pathway in Anti-CD40 Colitis Mice.Inflammatory bowel diseases · 2024Article
- Monogenic deficiency in murine intestinal Cdc42 leads to mucosal inflammation that induces crypt dysplasia.Genes & diseases · 2024Article
- Bacterial infection promotes tumorigenesis of colorectal cancer via regulating CDC42 acetylation.PLoS pathogens · 2023Article
- Senescent cells perturb intestinal stem cell differentiation through Ptk7 induced noncanonical Wnt and YAP signaling.Nature communications · 2023Article
- Targeting of Cdc42 GTPase in regulatory T cells unleashes antitumor T-cell immunity.Journal for immunotherapy of cancer · 2022Article
- Non-enzymatic role of SOD1 in intestinal stem cell growth.Cell death & disease · 2022Article
- Colonic healing requires Wnt produced by epithelium as well as Tagln+ and Acta2+ stromal cells.Development (Cambridge, England) · 2022Article
- Targeting Cancer by Using Nanoparticles to Modulate RHO GTPase Signaling.Advances in experimental medicine and biology · 2022Article
- Targeting the cytoskeleton against metastatic dissemination.Cancer metastasis reviews · 2021Review
- Review
- An Overview of Potential Therapeutic Agents Targeting WNT/PCP Signaling.Handbook of experimental pharmacology · 2021Review
- Plasticity of Intestinal Epithelium: Stem Cell Niches and Regulatory Signals.International journal of molecular sciences · 2020Review
- Elevating EGFR-MAPK program by a nonconventional Cdc42 enhances intestinal epithelial survival and regeneration.JCI insight · 2020Article
- The Regulation of Intestinal Mucosal Barrier by Myosin Light Chain Kinase/Rho Kinases.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
20 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in the APC or β-catenin genes are well-established initiators of colorectal cancer, yet modifiers that facilitate the survival and progression of nascent tumor cells are not well defined. Using genetic and pharmacologic approaches in mouse colorectal cancer and human colorectal cancer xenograft models, we show that incipient intestinal tumor cells activate CDC42, an APC-interacting small GTPase, as a crucial step in malignant progression. In the mouse, Cdc42 ablation attenuated the tumorigenicity of mutant intestinal cells carrying single APC or β-catenin mutations. Similarly, human colorectal cancer with relatively higher levels of CDC42 activity was particularly sensitive to CDC42 blockade. Mechanistic studies suggested that Cdc42 may be activated at different levels, including at the level of transcriptional activation of the stem cell-enriched Rho family exchange factor Arhgef4. Our results indicate that early-stage mutant intestinal epithelial cells must recruit the pleiotropic functions of Cdc42 for malignant progression, suggesting its relevance as a biomarker and therapeutic target for selective colorectal cancer intervention.
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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.