ArticleOncogene2017
Epithelial-mesenchymal transition of ovarian cancer cells is sustained by Rac1 through simultaneous activation of MEK1/2 and Src signaling pathways.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 94 citations in OpenAlex.
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- The Role of Cysteine-Rich Protein 2 in Aortic Dissection: Implications for VSMC Phenotypic Modulation-CSRP2 Impedes the Progression of Aortic Dissection.Biomolecules · 2026Article
- Spatial transcriptomic profiling of ovarian clear cell carcinoma reveals heterogeneity in OXPHOS and EMT gradients.Nature communications · 2026Article
- Pre-operative circulating tumor cells predict worse treatment outcome in patients with high-grade serous ovarian cancer.Oncogene · 2026Article
- The Emerging Role of FAM171A2 in Gynecological Malignancies: Bioinformatic Insights from UCEC and Ovarian Cancer.International journal of molecular sciences · 2025Article
- Patient-derived extracellular matrix from decellularized high-grade serous ovarian carcinoma tissues as a biocompatible support for organoid growth.Translational oncology · 2025Article
- TRIB1 facilitates the proliferation and migration of ovarian cancer cells by inducing EMT progression.Histology and histopathology · 2025Article
- Artemisinin Inhibits Drug Resistance and Epithelial-Mesenchymal Transition in Cervical Cancer Cells via the Wnt/β-Catenin Signaling Pathway.Bulletin of experimental biology and medicine · 2025Article
- From Defense to Disease: How the Immune System Fuels Epithelial-Mesenchymal Transition in Ovarian Cancer.International journal of molecular sciences · 2025Review
- Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024Review
- Article
- Pan-cancer transcriptomic data of ABI1 transcript variants and molecular constitutive elements identifies novel cancer metastatic and prognostic biomarkers.Cancer biomarkers : section A of Disease markers · 2024Article
- The CXCR4 antagonist R54 targets epithelial-mesenchymal transition (EMT) in human ovarian cancer cells.PloS one · 2024Article
- FAP is critical for ovarian cancer cell survival by sustaining NF-κB activation through recruitment of PRKDC in lipid rafts.Cancer gene therapy · 2023Article
- Epigallocatechin-3-Gallate Prevents the Acquisition of a Cancer Stem Cell Phenotype in Ovarian Cancer Tumorspheres through the Inhibition of Src/JAK/STAT3 Signaling.Biomedicines · 2023Article
- An EMT-based gene signature enhances the clinical understanding and prognostic prediction of patients with ovarian cancers.Journal of ovarian research · 2023Article
- LACTB exerts tumor suppressor properties in epithelial ovarian cancer through regulation of Slug.Life science alliance · 2023Article
- Agent-based modeling predicts RAC1 is critical for ovarian cancer metastasis.Molecular biology of the cell · 2022Article
- Multiomics characterization implicates PTK7 in ovarian cancer EMT and cell plasticity and offers strategies for therapeutic intervention.Cell death & disease · 2022Article
- Role of ELMO1 in inflammation and cancer-clinical implications.Cellular oncology (Dordrecht, Netherlands) · 2022Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
- Expression of concern
Authors and funding
9 authors at 7 institutions in 2 countries.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) is regarded as a crucial contributing factor to cancer progression. Diverse factors have been identified as potent EMT inducers in ovarian cancer. However, molecular mechanism sustaining EMT of ovarian cancer cells remains elusive. Here we show that the presence of SOS1/EPS8/ABI1 complex is critical for sustained EMT traits of ovarian cancer cells. Consistent with the role of SOS1/EPS8/ABI1 complex as a Rac1-specific guanine nucleotide exchange factor, depleting Rac1 results in the loss of most of mesenchymal traits in mesenchymal-like ovarian cancer cells, whereas expressing constitutively active Rac1 leads to EMT in epithelial-like ovarian cancer cells. With the aid of clinically tested inhibitors targeting various EMT-associated signaling pathways, we show that only combined treatment of mitogen-activated extracellular signal-regulated kinase 1/2 (MEK1/2) and Src inhibitors can abolish constitutively active Rac1-led EMT and mesenchymal traits displayed by mesenchymal-like ovarian cancer cells. Further experiments also reveal that EMT can be induced in epithelial-like ovarian cancer cells by co-expressing constitutively active MEK1 and Src rather than either alone. As the activities of Erk and Src are higher in ovarian cancer cells with constitutively active Rac1, we conclude that Rac1 sustains ovarian cancer cell EMT through simultaneous activation of MEK1/2 and Src signaling pathways. Importantly, we demonstrate that combined use of MEK1/2 and Src inhibitors effectively suppresses development of intraperitoneal xenografts and prolongs the survival of ovarian cancer-bearing mice. This study suggests that cocktail of MEK1/2 and Src inhibitors represents an effective therapeutic strategy against ovarian cancer progression.
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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.