ArticleGenes & cancer2013
The Role of Ect2 Nuclear RhoGEF Activity in Ovarian Cancer Cell Transformation.
Article in Genes & cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 68 citations in OpenAlex.
- Early induction of the Rho-GEF ECT2 drives MEK/ERK oncogenic signaling in pancreatic ductal adenocarcinoma.Oncogene · 2026Article
- RBM15 Enhances 5-Fluorouracil Drug Sensitivity and Suppresses Gastric Cancer Progression by Modulating N6-Methyladenosine Modification of ECT2-Dependent IGF2BP3.Research (Washington, D.C.) · 2026Article
- Cytoplasmic anillin and Ect2 promote RhoA/myosin II-dependent confined migration and invasion.Nature materials · 2025Article
- Research progress of ECT2 and RhoA-related signaling pathways in gynecological tumors.Frontiers in cell and developmental biology · 2025Review
- Identification of hub genes and pathways in Uterine corpus endometrial carcinoma (UCEC): A comprehensiveBiochemistry and biophysics reports · 2024Article
- New Mechanisms Underlying Oncogenesis in Dbl Family Rho Guanine Nucleotide Exchange Factors.Molecular pharmacology · 2024Review
- RBFOX2 deregulation promotes pancreatic cancer progression and metastasis through alternative splicing.Nature communications · 2023Article
- RHOAScience signaling · 2023Article
- Integration of Chemoinformatics and Multi-Omics Analysis Defines ECT2 as a Potential Target for Cancer Drug Therapy.Biology · 2023Article
- Cytokinesis machinery promotes cell dissociation from collectively migrating strands in confinement.Science advances · 2023Article
- Increased expression of ECT2 predicts the poor prognosis of breast cancer patients.Experimental hematology & oncology · 2022Article
- Activation Mechanism of RhoA Caused by Constitutively Activating Mutations G14V and Q63L.International journal of molecular sciences · 2022Article
- Role of the Hippo pathway in liver regeneration and repair: recent advances.Inflammation and regeneration · 2022Review
- DNA-PK promotes activation of the survival kinase AKT in response to DNA damage through an mTORC2-ECT2 pathway.Science signaling · 2022Article
- Aberrant Expression and Subcellular Localization of ECT2 Drives Colorectal Cancer Progression and Growth.Cancer research · 2022Article
- Transcriptional and epigenetic landscape of CaJournal of cell communication and signaling · 2021Article
- Epithelial cell transforming 2 is regulated by Yes-associated protein 1 and mediates pancreatic cancer progression and metastasis.American journal of physiology. Gastrointestinal and liver physiology · 2021Article
- Role of Small GTPase RhoA in DNA Damage Response.Biomolecules · 2021Review
- ECT2 promotes lung adenocarcinoma progression through extracellular matrix dynamics and focal adhesion signaling.Cancer science · 2021Article
- SmgGDS: An Emerging Master Regulator of Prenylation and Trafficking by Small GTPases in the Ras and Rho Families.Frontiers in molecular biosciences · 2021Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Ect2, a Rho guanine nucleotide exchange factor (RhoGEF), is atypical among RhoGEFs in its predominantly nuclear localization in interphase cells. One current model suggests that Ect2 mislocalization drives cellular transformation by promoting aberrant activation of cytoplasmic Rho family GTPase substrates. However, in ovarian cancers, where Ect2 is both amplified and overexpressed at the mRNA level, we observed that the protein is highly expressed and predominantly nuclear and that nuclear but not cytoplasmic Ect2 increases with advanced disease. Knockdown of Ect2 in ovarian cancer cell lines impaired their anchorage-independent growth without affecting their growth on plastic. Restoration of Ect2 expression rescued the anchorage-independent growth defect, but not if either the DH catalytic domain or the nuclear localization sequences of Ect2 were mutated. These results suggested a novel mechanism whereby Ect2 could drive transformation in ovarian cancer cells by acting as a RhoGEF specifically within the nucleus. Interestingly, Ect2 had an intrinsically distinct GTPase specificity profile in the nucleus versus the cytoplasm. Nuclear Ect2 bound preferentially to Rac1, while cytoplasmic Ect2 bound to RhoA but not Rac. Consistent with nuclear activation of endogenous Rac, Ect2 overexpression was sufficient to recruit Rac effectors to the nucleus, a process that required a functional Ect2 catalytic domain. Furthermore, expression of active nuclearly targeted Rac1 rescued the defect in transformed growth caused by Ect2 knockdown. Our work suggests a novel mechanism of Ect2-driven transformation, identifies subcellular localization as a regulator of GEF specificity, and implicates activation of nuclear Rac1 in cellular transformation.
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