ArticleBreast cancer research and treatment2010
Growth factor-induced resistance to tamoxifen is associated with a mutation of estrogen receptor alpha and its phosphorylation at serine 305.
Article in Breast cancer research and treatment, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- Non-coding RNA-mediated mechanisms underlying tamoxifen resistance in breast cancer.Discover oncology · 2026Review
- Evidence that CRISPR-Cas9 Y537S-mutant expressing breast cancer cells activate Yes-associated protein 1 to driving the conversion of normal fibroblasts into cancer-associated fibroblasts.Cell communication and signaling : CCS · 2024Article
- The intersection of the HER2-low subtype with endocrine resistance: the role of interconnected signaling pathways.Frontiers in oncology · 2024Article
- Identification of a human estrogen receptor α tetrapeptidic fragment with dual antiproliferative and anti-nociceptive action.Scientific reports · 2023Article
- Review
- A Closer Look at Estrogen Receptor Mutations in Breast Cancer and Their Implications for Estrogen and Antiestrogen Responses.International journal of molecular sciences · 2021Review
- Review
- The NF-κB Pathway Promotes Tamoxifen Tolerance and Disease Recurrence in Estrogen Receptor-Positive Breast Cancers.Molecular cancer research : MCR · 2020Article
- Insights into how phosphorylation of estrogen receptor at serine 305 modulates tamoxifen activity in breast cancer.Molecular and cellular endocrinology · 2019Review
- The Impact of ESR1 Mutations on the Treatment of Metastatic Breast Cancer.Hormones & cancer · 2018Review
- ESR1 mutations affect anti-proliferative responses to tamoxifen through enhanced cross-talk with IGF signaling.Breast cancer research and treatment · 2016Article
- Emerging roles of lysine methylation on non-histone proteins.Cellular and molecular life sciences : CMLS · 2015Review
- ESR1 mutations—a mechanism for acquired endocrine resistance in breast cancer.Nature reviews. Clinical oncology · 2015Review
- Minireview: Tipping the balance: ligand-independent activation of steroid receptors.Molecular endocrinology (Baltimore, Md.) · 2015Review
- The SMRT coregulator enhances growth of estrogen receptor-α-positive breast cancer cells by promotion of cell cycle progression and inhibition of apoptosis.Endocrinology · 2014Article
- Modeling luminal breast cancer heterogeneity: combination therapy to suppress a hormone receptor-negative, cytokeratin 5-positive subpopulation in luminal disease.Breast cancer research : BCR · 2014Article
- Estrogen receptor (ER) α mutations in breast cancer: hidden in plain sight.Breast cancer research and treatment · 2014Review
- Leptin increases HER2 protein levels through a STAT3-mediated up-regulation of Hsp90 in breast cancer cells.Molecular oncology · 2013Article
- Bergapten induces ER depletion in breast cancer cells through SMAD4-mediated ubiquitination.Breast cancer research and treatment · 2012Article
- Ligand binding promotes CDK-dependent phosphorylation of ER-alpha on hinge serine 294 but inhibits ligand-independent phosphorylation of serine 305.Molecular cancer research : MCR · 2012Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Estrogens play a crucial role in breast tumor growth, which is the rationale for the use of antiestrogens, such as tamoxifen, in women with estrogen receptor (ER)-alpha-positive breast cancer. However, hormone resistance is a major clinical problem. Altered growth factor signaling to the ERalpha pathway has been shown to be associated with the development of clinical resistance. We previously have identified a mutation that replaces arginine for lysine at residue 303 (K303R) of ERalpha, which confers hypersensitive growth in low levels of estrogen. To determine if the K303R mutation could participate in the evolution of hormone resistance, we generated MCF-7 breast cancer cells stably transfected with either wild-type (WT) or K303R ERalpha. We found that the mutation confers decreased sensitivity to tamoxifen in the presence of the growth factor heregulin, using anchorage-independent growth assays. K303R ERalpha-expressing cells were hypersensitive to growth factor signals. Our data suggest that phosphorylation of serine 305 within the hinge domain of ERalpha might play a key role in increasing ligand-independent activity of the mutant receptor. We hypothesize that the mutation adapts the receptor for enhanced bidirectional cross-talk with the HER2 growth factor receptor pathway, which then impacts on responsiveness to tamoxifen.
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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.