ArticleOncogene2017
The Cdc42/Rac1 regulator CdGAP is a novel E-cadherin transcriptional co-repressor with Zeb2 in breast cancer.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 40 citations in OpenAlex.
- Rho GTPases signaling mediates aggressiveness and differentiation in neuroblastoma tumors.Cell communication and signaling : CCS · 2026Article
- Pan-cancer signaling landscape linked to endothelial and immune Sphingosine-1-phosphate receptor 1 (S1PR1) expression.In silico pharmacology · 2026Article
- Dysregulated Polarized Secretion of Small Extracellular Vesicles in the Retinal Pigment Epithelium: Mechanisms and Pathological Roles in Age-Related Macular Degeneration.Journal of inflammation research · 2026Review
- Rac1 in gastric cancer: a molecular driver of invasion, EMT, and therapeutic resistance.Journal of translational medicine · 2025Review
- Rabenosyn-5 suppresses non-small cell lung cancer metastasis via inhibiting CDC42 activity.Cancer gene therapy · 2024Article
- CBX4 plays a bidirectional role in transcriptional regulation and lung adenocarcinoma progression.Cell death & disease · 2024Article
- CdGAP maintains podocyte function and modulates focal adhesions in a Src kinase-dependent manner.Scientific reports · 2022Article
- 4sc-202 and Ink-128 cooperate to reverse the epithelial to mesenchymal transition in OSCC.Oral diseases · 2022Article
- Fixing the GAP: The role of RhoGAPs in cancer.European journal of cell biology · 2022Review
- Circ_0000189 Promotes the Malignancy of Glioma Cells via Regulating miR-192-5p-ZEB2 Axis.Oxidative medicine and cellular longevity · 2022Article
- The emerging roles of srGAPs in cancer.Molecular biology reports · 2022Review
- CdGAP promotes prostate cancer metastasis by regulating epithelial-to-mesenchymal transition, cell cycle progression, and apoptosis.Communications biology · 2021Article
- ARHGAP10 inhibits the epithelial-mesenchymal transition of non-small cell lung cancer by inactivating PI3K/Akt/GSK3β signaling pathway.Cancer cell international · 2021Article
- MEF2A transcriptionally upregulates the expression of ZEB2 and CTNNB1 in colorectal cancer to promote tumor progression.Oncogene · 2021Article
- Advantages of Restoring miR-205-3p Expression for Better Prognosis of Gastric Cancer via Prevention of Epithelial-mesenchymal Transition.Journal of gastric cancer · 2020Article
- Death Domain-Associated Protein Promotes Colon Cancer Metastasis through Direct Interaction with ZEB1.Journal of Cancer · 2020Article
- METTL3-mediated N6-methyladenosine modification is critical for epithelial-mesenchymal transition and metastasis of gastric cancer.Molecular cancer · 2019Article
- Synaptotagmin 7 in twist-related protein 1-mediated epithelial - Mesenchymal transition of non-small cell lung cancer.EBioMedicine · 2019Article
- Silencing of hsa_circ_0004771 inhibits proliferation and induces apoptosis in breast cancer through activation of miR-653 by targeting ZEB2 signaling pathway.Bioscience reports · 2019Article
- The PAX6-ZEB2 axis promotes metastasis and cisplatin resistance in non-small cell lung cancer through PI3K/AKT signaling.Cell death & disease · 2019Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
The loss of E-cadherin causes dysfunction of the cell-cell junction machinery, which is an initial step in epithelial-to-mesenchymal transition (EMT), facilitating cancer cell invasion and the formation of metastases. A set of transcriptional repressors of E-cadherin (CDH1) gene expression, including Snail1, Snail2 and Zeb2 mediate E-cadherin downregulation in breast cancer. However, the molecular mechanisms underlying the control of E-cadherin expression in breast cancer progression remain largely unknown. Here, by using global gene expression approaches, we uncover a novel function for Cdc42 GTPase-activating protein (CdGAP) in the regulation of expression of genes involved in EMT. We found that CdGAP used its proline-rich domain to form a functional complex with Zeb2 to mediate the repression of E-cadherin expression in ErbB2-transformed breast cancer cells. Conversely, knockdown of CdGAP expression led to a decrease of the transcriptional repressors Snail1 and Zeb2, and this correlated with an increase in E-cadherin levels, restoration of cell-cell junctions, and epithelial-like morphological changes. In vivo, loss of CdGAP in ErbB2-transformed breast cancer cells impaired tumor growth and suppressed metastasis to lungs. Finally, CdGAP was highly expressed in basal-type breast cancer cells, and its strong expression correlated with poor prognosis in breast cancer patients. Together, these data support a previously unknown nuclear function for CdGAP where it cooperates in a GAP-independent manner with transcriptional repressors to function as a critical modulator of breast cancer through repression of E-cadherin transcription. Targeting Zeb2-CdGAP interactions may represent novel therapeutic opportunities for breast cancer treatment.
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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.