ArticleMolecular and cellular endocrinology2010
Estrogen receptor alpha 46 is reduced in tamoxifen resistant breast cancer cells and re-expression inhibits cell proliferation and estrogen receptor alpha 66-regulated target gene transcription.
Article in Molecular and cellular endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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
36 citing papers in PubMed, 84 citations in OpenAlex.
- Nucleic sexual hormone receptor signaling pathways in breast cancer: function regulation, crosstalk, and therapeutic implications.NPJ precision oncology · 2026Review
- Targeting estrogen receptor alpha in breast cancer for novel therapies resistance mechanisms and future directions.Discover oncology · 2025Review
- Genetic and epigenetic contribution to tamoxifen resistance in breast cancer, concepts to drive therapeutic strategies.Discover oncology · 2025Review
- miRNAs as emerging predictors of tamoxifen resistance in breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- miRNA-dependent resistance mechanisms to anti-hormonal therapies in estrogen receptor-positive breast cancer patients.Molecular therapy. Oncology · 2025Review
- Decoding estrogen receptor and GPER biology: structural insights and therapeutic advances in ERα-positive breast cancer.Frontiers in oncology · 2025Review
- dCas9-HDAC8-EGFP fusion enables epigenetic editing of breast cancer cells by H3K9 deacetylation.European journal of cell biology · 2024Article
- Estrogen Receptor Alpha Mutations, Truncations, Heterodimers, and Therapies.Endocrinology · 2024Review
- Overview of the therapeutic strategies for ER positive breast cancer.Biochemical pharmacology · 2023Review
- The Role of Different Types of microRNA in the Pathogenesis of Breast and Prostate Cancer.International journal of molecular sciences · 2023Review
- Molecular Mechanisms of Anti-Estrogen Therapy Resistance and Novel Targeted Therapies.Cancers · 2022Review
- The Isoforms of Estrogen Receptor Alpha and Beta in Thyroid Cancer.Frontiers in oncology · 2022Review
- Dissecting the Roles of PDCD4 in Breast Cancer.Frontiers in oncology · 2022Review
- Estrogen receptor-α signaling in post-natal mammary development and breast cancers.Cellular and molecular life sciences : CMLS · 2021Review
- Review
- EZH2 knockdown in tamoxifen-resistant MCF-7 cells unravels novel targets for regaining sensitivity towards tamoxifen.Breast cancer (Tokyo, Japan) · 2021Article
- Article
- Aberrant alternative splicing in breast cancer.Journal of molecular cell biology · 2019Review
- microRNA Regulation in Estrogen Receptor-Positive Breast Cancer and Endocrine Therapy.Biological procedures online · 2018Review
- Estrogen receptor expression in chronic hepatitis C and hepatocellular carcinoma pathogenesis.World journal of gastroenterology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Resistance to endocrine therapy is a major clinical problem in breast cancer. The role of ERalpha splice variants in endocrine resistance is largely unknown. We observed reduced protein expression of an N-terminally truncated ERalpha46 in endocrine-resistant LCC2, LCC9, and LY2 compared to MCF-7 breast cancer cells. Transfection of LCC9 and LY2 cells with hERalpha46 partially restored growth inhibition by TAM. Overexpression of hERalpha46 in MCF-7 cells reduced estradiol (E(2))-stimulated endogenous pS2, cyclin D1, nuclear respiratory factor-1 (NRF-1), and progesterone receptor transcription. Expression of oncomiR miR-21 was lower in TAM-resistant LCC9 and LY2 cells compared to MCF-7 cells. Transfection with ERalpha46 altered the pharmacology of E(2) regulation of miR-21 expression from inhibition to stimulation, consistent with the hypothesis that hERalpha46 inhibits ERalpha activity. Established miR-21 targets PTEN and PDCD4 were reduced in ERalpha46-transfected, E(2)-treated MCF-7 cells. In conclusion, ERalpha46 appears to enhance endocrine responses by inhibiting selected ERalpha66 responses.
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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.