ArticleJournal of cancer research and clinical oncology2010
Changes in expression, and/or mutations in TGF-beta receptors (TGF-beta RI and TGF-beta RII) and Smad 4 in human ovarian tumors.
Article in Journal of cancer research and clinical oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Target-Based Small Molecule Drug Discovery for Colorectal Cancer: A Review of Molecular Pathways and In Silico Studies.Biomolecules · 2022Review
- Correlation between Oxidative Stress and Transforming Growth Factor-Beta in Cancers.International journal of molecular sciences · 2021Review
- Transforming Growth Factor-Cancers · 2021Review
- Consequences of Mutations and Abnormal Expression of SMAD4 in Tumors and T Cells.OncoTargets and therapy · 2021Review
- Overexpressed VEPH1 inhibits epithelial-mesenchymal transition, invasion, and migration of human cutaneous melanoma cells through inactivating the TGF-β signaling pathway.Cell cycle (Georgetown, Tex.) · 2019Article
- Review
- Review
- TGFβ Controls Ovarian Cancer Cell Proliferation.International journal of molecular sciences · 2017Review
- Mesothelial-to-mesenchymal transition as a possible therapeutic target in peritoneal metastasis of ovarian cancer.The Journal of pathology · 2017Article
- Assessment of variation in immunosuppressive pathway genes reveals TGFBR2 to be associated with risk of clear cell ovarian cancer.Oncotarget · 2016Article
- Expression and clinical significance of cortactin protein in ovarian neoplasms.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2016Article
- Role of dihydrotestosterone (DHT) on TGF-β1 signaling pathway in epithelial ovarian cancer cells.Journal of cancer research and clinical oncology · 2016Article
- Epigenetic regulation of Smad2 and Smad3 by profilin-2 promotes lung cancer growth and metastasis.Nature communications · 2015Article
- Human ortholog of Drosophila Melted impedes SMAD2 release from TGF-β receptor I to inhibit TGF-β signaling.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The Immune Adaptor ADAP Regulates Reciprocal TGF-β1-Integrin Crosstalk to Protect from Influenza Virus Infection.PLoS pathogens · 2015Article
- TGF-β - an excellent servant but a bad master.Journal of translational medicine · 2012Review
- BRCA1 regulates follistatin function in ovarian cancer and human ovarian surface epithelial cells.PloS one · 2012Article
- Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeLoss of sensitivity to transforming growth factor beta (TGF-beta) signaling typically occurs in human ovarian cancer cells, but there is paucity of information regarding this in human ovarian tumors. Thus the association of inactivating mutations and/or variations in expression levels of TGF-beta signaling components with human ovarian tumors was evaluated.
methodsForty human ovarian tissue samples were analyzed for mutations and/or variations in the expression of transforming growth factor beta signaling components. Mutation studies were done through reverse transcription (RT) PCR, single strand conformation polymorphism analysis and automated DNA sequencing. Expression studies were carried out by semi quantitative RT PCR and western blotting. DNA binding ability of Smad complexes and expression of downstream targets were also analyzed.
resultsThe six alanine repeat containing variant of TGF-beta RI was seen in 27% of the tumor cases studied, in addition to the 45 bp nucleotide deletions in exon 1 of the receptor in two ovarian tumor samples. A deletion in the polyadenine tract of exon 3 of TGF-beta RII was seen in 22% of the tumor samples. We also report a loss or decrease in the expression of Smad 4 protein in tumor samples with a concurrent loss or reduced DNA binding ability of the Smad complex and deregulated expression of p21 and c-Myc.
conclusionsOur results suggest that mutations and/or alterations in expression of TGF-beta receptors and loss of Smad 4 are frequent in human ovarian cancers and may potentially explain the frequent loss of TGF-beta responsiveness that typically occurs in human ovarian cancer.
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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.