ArticleOncogene2002
Estrogen-like effects of thyroid hormone on the regulation of tumor suppressor proteins, p53 and retinoblastoma, in breast cancer cells.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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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
53 citing papers in PubMed, 123 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
- Serum Levels of Thyroid Hormones in Relation to Breast Cancer Prognosis: A Multicentre Cohort Study.Cancer medicine · 2026Article
- Thyroid Disease and Breast Cancer Risk in the Sister Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026Article
- Association between Benign Thyroid Disorders and Breast Cancer Risk in Korean Women.Cancer research and treatment · 2026Article
- Process to radioactive iodine treatment for Graves' hyperthyroidism: condemned or absolved?Journal of endocrinological investigation · 2025Review
- Hyperthyroidism and the risk of non-thyroid cancer: a Danish register-based long-term follow-up study.European thyroid journal · 2024Article
- FOXA1 Reprogramming Dictates Retinoid X Receptor Response in ESR1-Mutant Breast Cancer.Molecular cancer research : MCR · 2023Article
- Cancer and Mortality Risks of Graves' Disease in South Korea Based on National Data from 2010 to 2019.Clinical epidemiology · 2023Article
- Mediator subunit MED1 differentially modulates mutant thyroid hormone receptor intracellular dynamics in Resistance to Thyroid Hormone syndrome.Molecular and cellular endocrinology · 2023Article
- Links between Breast and Thyroid Cancer: Hormones, Genetic Susceptibility and Medical Interventions.Cancers · 2022Review
- Hormonal Crosstalk Between Thyroid and Breast Cancer.Endocrinology · 2022Review
- The TSH/Thyroid Hormones Axis and Breast Cancer.Journal of clinical medicine · 2022Review
- Association between Thyroid Cancer and Breast Cancer: Two Longitudinal Follow-Up Studies Using a National Health Screening Cohort.Journal of personalized medicine · 2022Article
- Low thyroid hormone receptor alpha-2 (THRα-2) tumor expression is associated with unfavorable tumor characteristics and high breast cancer mortality.Breast cancer research : BCR · 2021Article
- Risk Factors of Synchronous Breast and Thyroid Cancer: a Controlled Multicenter Study and Review of the Literature.Materia socio-medica · 2021Review
- Article
- Schisandrol A Exhibits Estrogenic Activity via Estrogen Receptor α-Dependent Signaling Pathway in Estrogen Receptor-Positive Breast Cancer Cells.Pharmaceutics · 2021Article
- The Prognostic Impact of Retinoid X Receptor and Thyroid Hormone Receptor alpha in Unifocal vs. Multifocal/Multicentric Breast Cancer.International journal of molecular sciences · 2021Article
- Early Life Exposure to Aflatoxin B1 in Rats: Alterations in Lipids, Hormones, and DNA Methylation among the Offspring.International journal of environmental research and public health · 2021Article
- Correlation Analysis of Breast and Thyroid Nodules: A Cross-Sectional Study.International journal of general medicine · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T47D cells represent an estrogen-responsive human ductal carcinoma cell line which expresses detectable levels of estrogen receptor (ER). We have previously shown that estradiol (E(2)) treatment of T47D cells causes an increase in the level of p53 and a concomitant phosphorylation of retinoblastoma protein (pRb). In the present study, we have analysed the expression of p53 and phosphorylation state of pRb and compared the effects of E(2) and triiodothyronine (T(3)) on these phenomena. Cells were grown in a medium containing charcoal-treated serum to deplete the levels of endogenous steroids. Upon confluency, the cells were treated with T(3) (10(-12) to 10(-7) M) for 24 h and the presence of p53 and pRb was detected by Western analysis. E(2) treatment of cells caused a 2-3-fold increase in the level of p53. Presence of T(3) in the medium caused a gradual increase in the level of p53 in a concentration-dependent manner. Under the above conditions, pRb was phosphorylated (detected as an upshift during SDS-PAGE) in the presence of E(2) and T(3). Supplementation of growth medium with T(3) (1 microM) caused an increase in the rate of proliferation of T47D cells and induced hyperphosphorylation of pRb within 4 h; this effect was maintained for up to 12 h. When ICI 164 384 (ICI) (1 microM), an ER antagonist, was combined with E(2) (1 nM) or T(3) (1 microM), effects of hormones on cell proliferation and hyperphosphorylation of pRb were blocked. Western analysis of p53 was supplemented with its cytolocalization by immuno-labeling using laser scanning confocal fluorescence microscopy, which revealed an ICI-sensitive increase in the abundance of p53 in hormone-treated cells. Steroid binding analysis revealed lack of competition by T(3) for the [(3)H]E(2) binding. These results indicate that T(3) regulates T47D cell cycle progression and proliferation raising the p53 level and causing hyperphosphorylation of pRb by a common mechanism involving ER and T(3) receptor (T(3)R)-mediated pathways.
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