ArticleTheScientificWorldJournal2014
Estrogen-responsive genes overlap with triiodothyronine-responsive genes in a breast carcinoma cell line.
Article in TheScientificWorldJournal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Thyroid function alters during neoadjuvant chemotherapy in breast cancer patients: results from the NEOZOTAC trial (BOOG 2010-01).Breast cancer research and treatment · 2015Trial
- Triiodothyronine (T3) increases the expression of the amphiregulin (AREG) oncogene by activating extranuclear pathways in MCF-7 breast cancer cells.Archives of endocrinology and metabolism · 2024Article
- Review
- Hormonal Crosstalk Between Thyroid and Breast Cancer.Endocrinology · 2022Review
- A New Perspective on Thyroid Hormones: Crosstalk with Reproductive Hormones in Females.International journal of molecular sciences · 2022Review
- Claudin 6: Therapeutic prospects for tumours, and mechanisms of expression and regulation (Review).Molecular medicine reports · 2021Review
- Higher order genomic organization and epigenetic control maintain cellular identity and prevent breast cancer.Genes, chromosomes & cancer · 2019Review
- Triiodothyronine Promotes Cell Proliferation of Breast Cancer via Modulating miR-204/Amphiregulin.Pathology oncology research : POR · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been well established that estrogen plays an important role in the progression and treatment of breast cancer. However, the role of triiodothyronine (T₃) remains controversial. We have previously shown its capacity to stimulate the development of positive estrogen receptor breast carcinoma, induce the expression of genes (PR, TGF-alpha) normally stimulated by estradiol (E₂), and suppress genes (TGF-beta) normally inhibited by E₂. Since T₃ regulates growth hormones, metabolism, and differentiation, it is important to verify its action on other genes normally induced by E₂. Therefore, we used DNA microarrays to compare gene expression patterns in MCF-7 breast adenocarcinoma cells treated with E₂ and T₃. Several genes were modulated by both E₂ and T₃ in MCF-7 cells (Student's t-test, P < 0.05). Specifically, we found eight genes that were differentially expressed after treatment with both E₂ and T₃, including amphiregulin, fibulin 1, claudin 6, pericentriolar material 1, premature ovarian failure 1B, factor for adipocyte differentiation-104, sterile alpha motif domain containing 9, and likely ortholog of rat vacuole membrane protein 1 (fold change > 2.0, pFDR < 0.05). We confirmed our microarray results by real-time PCR. Our findings reveal that certain genes in MCF-7 cells can be regulated by both E₂ and T₃.
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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.