ArticleCancer biology & therapy2019
Inhibition of Cdc42-intersectin interaction by small molecule ZCL367 impedes cancer cell cycle progression, proliferation, migration, and tumor growth.
Article in Cancer biology & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Rho GTPases in cancer resistance: mechanisms, vulnerabilities, and therapeutic opportunities.Biochemical Society transactions · 2026Review
- Targeting Cdc42: Novel Approaches in Cardiovascular Disorders.Current protein & peptide science · 2026Review
- Inhibition of CDC42 in adenomyosis reduces the proliferation of endometrial stromal cells and the migration of epithelial cells.American journal of translational research · 2026Article
- Rho Small GTPase Family in Androgen-Regulated Prostate Cancer Progression and Metastasis.Cancers · 2025Review
- Methods for Controlling Small GTPase Activity.Chembiochem : a European journal of chemical biology · 2025Review
- Tetrandrine induces cell cycle arrest in cutaneous melanoma cells by inhibiting IL-6/CDC42 signaling.Archives of dermatological research · 2025Article
- Enabling systemic identification and functionality profiling for Cdc42 homeostatic modulators.Communications chemistry · 2024Article
- Discovery of CDC42 Inhibitors with a Favorable Pharmacokinetic Profile and Anticancer In Vivo Efficacy.Journal of medicinal chemistry · 2024Article
- Molecular dynamics simulations reveal the inhibition mechanism of Cdc42 by RhoGDI1.Journal of computer-aided molecular design · 2023Article
- Targeting small GTPases: emerging grasps on previously untamable targets, pioneered by KRAS.Signal transduction and targeted therapy · 2023Review
- Review
- Podocalyxin-Like Protein 1 Regulates Pluripotency through the Cholesterol Biosynthesis Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- lncRNA DSCR8 mediates miR-137/Cdc42 to regulate gastric cancer cell proliferation, invasion, and cell cycle as a competitive endogenous RNA.Molecular therapy oncolytics · 2021Article
- Progress in the therapeutic inhibition of Cdc42 signalling.Biochemical Society transactions · 2021Review
- Bioinformatic Prediction of Signaling Pathways for Apurinic/Apyrimidinic Endodeoxyribonuclease 1 (APEX1) and Its Role in Cholangiocarcinoma Cells.Molecules (Basel, Switzerland) · 2021Article
- Selective axonal translation of the mRNA isoform encoding prenylated Cdc42 supports axon growth.Journal of cell science · 2021Article
- An Overview of Potential Therapeutic Agents Targeting WNT/PCP Signaling.Handbook of experimental pharmacology · 2021Review
- Pharmacological Modulators of Small GTPases of Rho Family in Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Article
- Review
- Dysregulation of Rho GTPases in Human Cancers.Cancers · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Cdc42 is a member of the Rho family of small GTPases that are at the crossroads of major oncogenic signaling pathways involved in both lung and prostate cancers. However, the therapeutic potential of Cdc42 regulation is still unclear due to the lack of pharmacological tools. Herein, we report that ZCL367 is a bona fide Cdc42 inhibitor that suppressed cancer development and ZCL278 can act as a partial Cdc42 agonist. In lung cancer cell lines with varying EGFR and Ras mutations as well as both androgen-independent and androgen-dependent prostate cancer cell lines, ZCL367 impeded cell cycle progression, reduced proliferation, and suppressed migration. ZCL367 decreased Cdc42-intersectin interactions and reduced Cdc42-mediated filopodia formation. ZCL367 showed increased potency and selectivity for Cdc42 when compared to Rac1 and RhoA. ZCL367 reduced A549 tumorigenesis in a xenograft mouse model. Altogether, ZCL367 is a selective Cdc42 inhibitor and an excellent candidate for lead compound optimization for further anticancer studies.
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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.