ArticleNeoplasia (New York, N.Y.)2008
Aberrant transforming growth factor beta1 signaling and SMAD4 nuclear translocation confer epigenetic repression of ADAM19 in ovarian cancer.
Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 66 citations in OpenAlex.
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- IER3: exploring its dual function as an oncogene and tumor suppressor.Cancer gene therapy · 2025Article
- The silent spread: exploring diverse metastatic pathways in high-grade serous ovarian cancer.Frontiers in medicine · 2025Review
- Transcriptomic Analysis of Hub Genes Reveals Associated Inflammatory Pathways in Estrogen-Dependent Gynecological Diseases.Biology · 2024Article
- Clinical Significance of the Immunohistochemical Expression of Histone Deacetylases (HDACs)-2, -4, and -5 in Ovarian Adenocarcinomas.Biomedicines · 2024Article
- Genome-wide mapping of somatic mutation rates uncovers drivers of cancer.Nature biotechnology · 2022Article
- Comparing the Secretomes of Chemorefractory and Chemoresistant Ovarian Cancer Cell Populations.Cancers · 2022Review
- Role of non-coding RNAs and exosomal non-coding RNAs in retinoblastoma progression.Frontiers in cell and developmental biology · 2022Review
- Article
- Circular RNA has_circ_0000034 accelerates retinoblastoma advancement through the miR-361-3p/ADAM19 axis.Molecular and cellular biochemistry · 2021Article
- Endometriosis and ovarian cancer risk, an epigenetic connection.Annals of translational medicine · 2020Review
- Analysis of the clinical significance of DNA methylation in gastric cancer based on a genome-wide high-resolution array.Clinical epigenetics · 2019Article
- Epigenetic Biomarkers in the Management of Ovarian Cancer: Current Prospectives.Frontiers in cell and developmental biology · 2019Review
- Preliminary Study of the Role F-Box Protein 32 (FBXO32) in Colorectal Neoplasms Through the Transforming Growth Factor beta (TGF-β)/Smad4 Signalling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Overexpression of a disintegrin and metalloproteinase 21 is associated with motility, metastasis, and poor prognosis in hepatocellular carcinoma.Scientific reports · 2017Article
- MDM2 promotes epithelial-mesenchymal transition and metastasis of ovarian cancer SKOV3 cells.British journal of cancer · 2017Article
- Mesothelial-to-mesenchymal transition as a possible therapeutic target in peritoneal metastasis of ovarian cancer.The Journal of pathology · 2017Article
- Epigenetic silencing of the NR4A3 tumor suppressor, by aberrant JAK/STAT signaling, predicts prognosis in gastric cancer.Scientific reports · 2016Article
- Genetic and epigenetic heterogeneity of epithelial ovarian cancer and the clinical implications for molecular targeted therapy.Journal of cellular and molecular medicine · 2016Review
- Genetic and cellular studies highlight that A Disintegrin and Metalloproteinase 19 is a protective biomarker in human prostate cancer.BMC cancer · 2016Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Transforming growth factor-beta (TGF-beta)/SMAD signaling is a key growth regulatory pathway often dysregulated in ovarian cancer and other malignancies. Although loss of TGF-beta-mediated growth inhibition has been shown to contribute to aberrant cell behavior, the epigenetic consequence(s) of impaired TGF-beta/SMAD signaling on target genes is not well established. In this study, we show that TGF-beta1 causes growth inhibition of normal ovarian surface epithelial cells, induction of nuclear translocation SMAD4, and up-regulation of ADAM19 (a disintegrin and metalloprotease domain 19), a newly identified TGF-beta1 target gene. Conversely, induction and nuclear translocation of SMAD4 were negligible in ovarian cancer cells refractory to TGF-beta1 stimulation, and ADAM19 expression was greatly reduced. Furthermore, in the TGF-beta1 refractory cells, an inactive chromatin environment, marked by repressive histone modifications (trimethyl-H3K27 and dimethyl-H3K9) and histone deacetylase, was associated with the ADAM19 promoter region. However, the CpG island found within the promoter and first exon of ADAM19 remained generally unmethylated. Although disrupted growth factor signaling has been linked to epigenetic gene silencing in cancer, this is the first evidence demonstrating that impaired TGF-beta1 signaling can result in the formation of a repressive chromatin state and epigenetic suppression of ADAM19. Given the emerging role of ADAMs family proteins in growth factor regulation in normal cells, we suggest that epigenetic dysregulation of ADAM19 may contribute to the neoplastic process in 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.