ArticleOncogene2008
Difference between genomic actions of estrogen versus raloxifene in human ovarian cancer cell lines.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- PARAGON (ANZGOG-0903): a phase 2 study of anastrozole in asymptomatic patients with estrogen and progesterone receptor-positive recurrent ovarian cancer and CA125 progression.Journal of gynecologic oncology · 2019Trial
- Phlorotannins fromMarine drugs · 2025Article
- The multifaceted therapeutic value of targeting steroid receptor coactivator-1 in tumorigenesis.Cell & bioscience · 2024Review
- Nuclear receptor co-repressor NCOR2 and its relation to GPER with prognostic impact in ovarian cancer.Journal of cancer research and clinical oncology · 2023Article
- The Role of Cow's Milk Consumption in Breast Cancer Initiation and Progression.Current nutrition reports · 2023Review
- Malignant Ascites Promote Adhesion of Ovarian Cancer Cells to Peritoneal Mesothelium and Fibroblasts.International journal of molecular sciences · 2021Article
- Combinatorial PX-866 and Raloxifene Decrease Rb Phosphorylation, Cyclin E2 Transcription, and Proliferation of MCF-7 Breast Cancer Cells.Journal of cellular biochemistry · 2016Article
- Down-regulation of hTERT and Cyclin D1 transcription via PI3K/Akt and TGF-β pathways in MCF-7 Cancer cells with PX-866 and Raloxifene.Experimental cell research · 2016Article
- Phosphorylation-mediated EZH2 inactivation promotes drug resistance in multiple myeloma.The Journal of clinical investigation · 2015Article
- The Regulation of IGF-1 Gene Transcription and Splicing during Development and Aging.Frontiers in endocrinology · 2013Article
- Estradiol and raloxifene induce the proliferation of osteoblasts through G-protein-coupled receptor GPR30.Journal of endocrinological investigation · 2013Article
- BRCA1 negatively regulates IGF-1 expression through an estrogen-responsive element-like site.Cell death & disease · 2012Article
- Who's in charge? Nuclear receptor coactivator and corepressor function in brain and behavior.Frontiers in neuroendocrinology · 2009Review
- Role of Insulin-like Growth Factor, Insulin-like Growth Factor Receptors, and Insulin-like Growth Factor-binding Proteins in Ovarian Cancer.Indian journal of medical and paediatric oncology : official journal of Indian Society of Medical & Paediatric OncologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although there is growing evidence that estrogens promote tumor progression in epithelial ovarian cancer, the molecular mechanisms accounting for this are still unclear. Selective estrogen receptor modulators (SERMs) mimic estrogen action in certain tissues while opposing it in others. The molecular mechanisms of the effects of SERMs such as raloxifene on the tumor progression of epithelial ovarian cancer are also still unclear. Here, we show that various genomic actions of estrogen differ from those of raloxifene in human ovarian cancer cell lines expressing estrogen receptor alpha (ERalpha). 17beta-Estradiol (E2) induced the gene expression of c-Myc and IGF-1 and increased the binding of ERalpha to the AP1 site of the promoters of c-Myc and IGF-1. ERalpha silencing abolished the E2-stimulated c-Myc expression. E2 induced the recruitment of co-activators such as SRC-1, SRC-3 and CBP to the promoters of c-Myc and IGF-1, and SRC-1 silencing abolished both the E2-stimulated c-Myc expression and cell-cycle progression. In contrast, although raloxifene increased the binding of ERalpha to the AP1 site of the promoters of c-Myc and IGF-1, raloxifene had no effect on the gene expression of c-Myc or IGF-1. Raloxifene induced the recruitment of co-repressors such as HDAC2, N-CoR and SMRT to the promoter of IGF-1. Thus, the difference between the genomic actions exerted by estrogen and raloxifene in human ovarian cancer cell lines expressing ERalpha appear to be dependent on the recruitment of co-regulators.
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Registered trials
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.