ArticleMolecular cancer research : MCR2008
Transforming growth factor-beta1, transforming growth factor-beta2, and transforming growth factor-beta3 enhance ovarian cancer metastatic potential by inducing a Smad3-dependent epithelial-to-mesenchymal transition.
Article in Molecular cancer research : MCR, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
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Who cites it
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.
- Upregulated N-cadherin expression is associated with poor prognosis in epithelial-derived solid tumours: A meta-analysis.European journal of clinical investigation · 2018Pooled it
- Discovery and Development of a TGFβ3/IL-13 Plasma Risk Score for Preoperative Discrimination of Benign and Malignant Ovarian Adnexal Masses.Diagnostics (Basel, Switzerland) · 2026Article
- Bioinformatic Approach to Identify PotentialInternational journal of molecular sciences · 2025Article
- Epidemiology, molecular typing, microbiome-immune interactions and treatment strategies of endometrial cancer: a review.Frontiers in immunology · 2025Review
- A patient stratification signature mirrors the immunogenic potential of high grade serous ovarian cancers.Journal of translational medicine · 2024Article
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- Differential DNA Methylation and Gene Expression Between ALV-J-Positive and ALV-J-Negative Chickens.Frontiers in veterinary science · 2021Article
- TGF-β2 is a Prognostic Biomarker Correlated with Immune Cell Infiltration in Colorectal Cancer: A STROBE-compliant article.Medicine · 2020Observational
- TGFβ2 is a prognostic-related biomarker and correlated with immune infiltrates in gastric cancer.Journal of cellular and molecular medicine · 2020Article
- Abiraterone in patients with recurrent epithelial ovarian cancer: principal results of the phase II Cancer of the Ovary Abiraterone (CORAL) trial (CRUK - A16037).Therapeutic advances in medical oncology · 2020Article
- Prognostic Values of Transforming Growth Factor-Beta Subtypes in Ovarian Cancer.BioMed research international · 2020Article
- Corilagin in Cancer: A Critical Evaluation of Anticancer Activities and Molecular Mechanisms.Molecules (Basel, Switzerland) · 2019Review
- TGF-β1 and TNF-α synergistically induce epithelial to mesenchymal transition of breast cancer cells by enhancing TAK1 activation.Journal of cell communication and signaling · 2019Article
- Molecular mechanisms underlying mifepristone's agonistic action on ovarian cancer progression.EBioMedicine · 2019Article
- Naturally Killing the Silent Killer: NK Cell-Based Immunotherapy for Ovarian Cancer.Frontiers in immunology · 2019Review
- Exosomal miR-21-5p derived from gastric cancer promotes peritoneal metastasis via mesothelial-to-mesenchymal transition.Cell death & disease · 2018Article
- nc886 is induced by TGF-β and suppresses the microRNA pathway in ovarian cancer.Nature communications · 2018Article
- Histone Methyltransferase EZH2: A Therapeutic Target for Ovarian Cancer.Molecular cancer therapeutics · 2018Review
5 more citing papers are in PubMed but not listed here.
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5 authors at 2 institutions in 2 countries.
Funding
Abstract
Transforming growth factor-beta (TGF-beta) is thought to play a role in the pathobiological progression of ovarian cancer because this peptide hormone is overexpressed in cancer tissue, plasma, and peritoneal fluid. In the current study, we investigated the role of the TGF-beta/Smad3 pathway in ovarian cancer metastasis by regulation of an epithelial-to-mesenchymal transition. When cancer cells were cultured on plastic, TGF-beta1, TGF-beta2, and TGF-beta3 induced pro-matrix metalloproteinase (MMP) secretion, loss of cell-cell junctions, down-regulation of E-cadherin, up-regulation of N-cadherin, and acquisition of a fibroblastoid phenotype, consistent with an epithelial-to-mesenchymal transition. Furthermore, Smad3 small interfering RNA transfection inhibited TGF-beta-mediated changes to a fibroblastic morphology, but not MMP secretion. When cancer cells were cultured on a three-dimensional collagen matrix, TGF-beta1, TGF-beta2, and TGF-beta3 stimulated both pro-MMP and active MMP secretion and invasion. Smad3 small interfering RNA transfection of cells cultured on a collagen matrix abrogated TGF-beta-stimulated invasion and MMP secretion. Analysis of Smad3 nuclear expression in microarrays of serous benign tumors, borderline tumors, and cystadenocarcinoma revealed that Smad3 expression could be used to distinguish benign and borderline tumors from carcinoma (P = 0.006). Higher Smad3 expression also correlated with poor survival (P = 0.031). Furthermore, a direct relationship exists between Smad3 nuclear expression and expression of the mesenchymal marker N-cadherin in cancer patients (P = 0.0057). Collectively, these results implicate an important role for the TGF-beta/Smad3 pathway in mediating ovarian oncogenesis by enhancing metastatic potential.
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