ArticleCarcinogenesis2012
Med1 plays a critical role in the development of tamoxifen resistance.
Article in Carcinogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 61 citations in OpenAlex.
- Pausing for stress.Nature chemical biology · 2026Article
- MUC1-C dependency in drug resistant HR+/HER2- breast cancer identifies a new target for antibody-drug conjugate treatment.NPJ breast cancer · 2025Article
- miR-205 Regulates Tamoxifen Resistance by Targeting Estrogen Receptor Coactivator MED1 in Human Breast Cancer.Cancers · 2024Article
- Obesity, dysbiosis and inflammation: interactions that modulate the efficacy of immunotherapy.Frontiers in immunology · 2024Review
- Liquid‒liquid phase separation: roles and implications in future cancer treatment.International journal of biological sciences · 2023Review
- Review
- Learning the chemical grammar of biomolecular condensates.Nature chemical biology · 2022Review
- MED1, a novel binding partner of BRCA1, regulates homologous recombination and R-loop processing.Scientific reports · 2022Article
- Advances of Epigenetic Biomarkers and Epigenome Editing for Early Diagnosis in Breast Cancer.International journal of molecular sciences · 2022Review
- Liquid-liquid phase separation in tumor biology.Signal transduction and targeted therapy · 2022Review
- Review
- Transcriptional coactivator MED1 in the interface of anti-estrogen and anti-HER2 therapeutic resistance.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- Principles and functions of condensate modifying drugs.Frontiers in molecular biosciences · 2022Review
- Article
- HIF1α and p53 Regulated MED30, a Mediator Complex Subunit, is Involved in Regulation of Glioblastoma Pathogenesis and Temozolomide Resistance.Cellular and molecular neurobiology · 2021Article
- Hyperleptinemia in obese state renders luminal breast cancers refractory to tamoxifen by coordinating a crosstalk between Med1, miR205 and ErbB.NPJ breast cancer · 2021Article
- Functional cooperation between co-amplified genes promotes aggressive phenotypes of HER2-positive breast cancer.Cell reports · 2021Article
- Biomolecular Condensates and Cancer.Cancer cell · 2021Review
- Partitioning of cancer therapeutics in nuclear condensates.Science (New York, N.Y.) · 2020Article
- The Preparation of Ginsenoside Rg5, Its Antitumor Activity against Breast Cancer Cells and Its Targeting of PI3K.Nutrients · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 7 institutions in 3 countries.
Funding
Abstract
Understanding the molecular pathways that contribute to the development of tamoxifen resistance is a critical research priority as acquired tamoxifen resistance is the principal cause of poor prognosis and death of patients with originally good prognosis hormone-responsive breast tumors. In this report, we provide evidence that Med1, an important subunit of mediator coactivator complex, is spontaneously upregulated during acquired tamoxifen-resistance development potentiating agonist activities of tamoxifen. Phosphorylated Med1 and estrogen receptor (ER) are abundant in tamoxifen-resistant breast cancer cells due to persistent activation of extracellular signal-regulated kinases. Mechanistically, phosphorylated Med1 exhibits nuclear accumulation, increased interaction with ER and higher tamoxifen-induced recruitment to ER-responsive promoters, which is abrogated by inhibition of Med1 phosphorylation. Stable knockdown of Med1 in tamoxifen-resistant cells not only reverses tamoxifen resistance in vitro but also in vivo. Finally, higher expression levels of Med1 in the tumor significantly correlated with tamoxifen resistance in ER-positive breast cancer patients on adjuvant tamoxifen monotherapy. In silico analysis of breast cancer, utilizing published profiling studies showed that Med1 is overexpressed in aggressive subsets. These findings provide what we believe is the first evidence for a critical role for Med1 in tamoxifen resistance and identify this coactivator protein as an essential effector of the tamoxifen-induced breast cancer growth.
Indexed as
Identifiers
What OpenQuestion holds
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.