ArticleEMBO molecular medicine2019
Epigenetic silencing of SALL2 confers tamoxifen resistance in breast cancer.
Article in EMBO molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 83 citations in OpenAlex.
- Article
- Nucleic sexual hormone receptor signaling pathways in breast cancer: function regulation, crosstalk, and therapeutic implications.NPJ precision oncology · 2026Review
- Targeting epigenetic methylation: emerging diagnosis and therapeutic strategies in cancer.Experimental hematology & oncology · 2026Review
- Navigating the complexities of epigenetic dysregulation in breast cancer and its implication in therapeutic interventions: a comprehensive overview.Molecular and cellular biochemistry · 2026Review
- DNA methylation biomarkers for the diagnosis and treatment management of breast cancer: where are we now?Epigenomics · 2025Review
- Article
- The tumor suppressor SALL2 opposes chemotherapeutic resistance in breast cancer.Molecular and cellular biochemistry · 2025Article
- Triple-positive breast cancer: navigating heterogeneity and advancing multimodal therapies for improving patient outcomes.Cancer cell international · 2025Review
- Decoding breast cancer treatment resistance through genetic, epigenetic, and immune-regulatory mechanisms: from molecular insights to translational perspectives.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Crosstalk of methylation and tamoxifen in breast cancer (Review).Molecular medicine reports · 2024Review
- Article
- Selective Estrogen Receptor Modulators' (SERMs) Influence onInternational journal of molecular sciences · 2024Article
- Extracellular vesicles in anti-tumor drug resistance: Mechanisms and therapeutic prospects.Journal of pharmaceutical analysis · 2024Review
- SMAD4 depletion contributes to endocrine resistance by integrating ER and ERBB signaling in HR + HER2- breast cancer.Cell death & disease · 2024Article
- Isolation and Characterization of a Novel Mammary Adenocarcinoma, MCa-P1362, with Hormone Receptor Expression, Human Epidermal Growth Factor Receptor 2 Positivity, and Enrichment in Cancer and Mesenchymal Stem Cells.The American journal of pathology · 2024Article
- Leveraging a disulfidptosis/ferroptosis-based signature to predict the prognosis of lung adenocarcinoma.Cancer cell international · 2023Article
- Netrin-1 blockade inhibits tumor associated Myeloid-derived suppressor cells, cancer stemness and alleviates resistance to chemotherapy and immune checkpoint inhibitor.Cell death and differentiation · 2023Article
- The Mechanism of DNA Methylation and miRNA in Breast Cancer.International journal of molecular sciences · 2023Review
- Stilbenes: a promising small molecule modulator for epigenetic regulation in human diseases.Frontiers in pharmacology · 2023Review
- Emerging roles of endoplasmic reticulum stress in the cellular plasticity of cancer cells.Frontiers in oncology · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
19 authors at 3 institutions in 2 countries.
Funding
Abstract
Resistance to tamoxifen is a clinically major challenge in breast cancer treatment. Although downregulation of estrogen receptor-alpha (ERα) is the dominant mechanism of tamoxifen resistance, the reason for ERα decrease during tamoxifen therapy remains elusive. Herein, we reported that Spalt-like transcription factor 2 (SALL2) expression was significantly reduced during tamoxifen therapy through transcription profiling analysis of 9 paired primary pre-tamoxifen-treated and relapsed tamoxifen-resistant breast cancer tissues. SALL2 transcriptionally upregulated ESR1 and PTEN through directly binding to the DNA promoters. By contrast, silencing SALL2 induced downregulation of ERα and PTEN and activated the Akt/mTOR signaling, resulting in estrogen-independent growth and tamoxifen resistance in ERα-positive breast cancer. Furthermore, hypermethylation of SALL2 promoter was found in tamoxifen-resistant breast cancer. Importantly, in vivo experiments showed that DNA methyltransferase inhibitor-mediated SALL2 restoration resensitized tamoxifen-resistant breast cancer to tamoxifen therapy. These findings shed light on the mechanism of SALL2 in regulation of ER and represent a potential clinical signature that can be used to categorize breast cancer patients who may benefit from co-therapy with tamoxifen and DNMT inhibitor.
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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.