ArticleBreast cancer research and treatment2013
Fulvestrant regulates epidermal growth factor (EGF) family ligands to activate EGF receptor (EGFR) signaling in breast cancer cells.
Article in Breast cancer research and treatment, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Deacidification of the Endolysosomal System by the Vesicular Proton Pump V-ATPase Inhibitor Bafilomycin A1 Affects EGF Receptor Endocytosis Differently in Endometrial MSC and HeLa Cells.International journal of molecular sciences · 2025Article
- Network Pharmacology Approach and Experimental Verification to Explore the Anti-NSCLC Mechanism of Grifolic Acid.International journal of molecular sciences · 2025Article
- GZ17-6.02 and palbociclib interact to kill ER+ breast cancer cells.Oncotarget · 2022Article
- An H3K4me3 reader, BAP18 as an adaptor of COMPASS-like core subunits co-activates ERα action and associates with the sensitivity of antiestrogen in breast cancer.Nucleic acids research · 2020Article
- Fulvestrant in Combination with CDK4/6 Inhibitors for HER2- Metastatic Breast Cancers: Current Perspectives.Breast cancer (Dove Medical Press) · 2020Review
- Fulvestrant in the treatment of hormone receptor-positive/human epidermal growth factor receptor 2-negative advanced breast cancer: A review.Cancer medicine · 2019Review
- Extended Adjuvant Therapy with Neratinib Plus Fulvestrant Blocks ER/HER2 Crosstalk and Maintains Complete Responses of ERClinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Article
- Role of estrogen receptor alpha in human cervical cancer-associated fibroblasts: a transcriptomic study.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Tetratricopeptide repeat domain 9A negatively regulates estrogen receptor alpha activity.International journal of biological sciences · 2015Article
- Transactivation of epidermal growth factor receptor through platelet-activating factor/receptor in ovarian cancer cells.Journal of experimental & clinical cancer research : CR · 2014Article
- Overcoming endocrine resistance due to reduced PTEN levels in estrogen receptor-positive breast cancer by co-targeting mammalian target of rapamycin, protein kinase B, or mitogen-activated protein kinase kinase.Breast cancer research : BCR · 2014Article
- Fulvestrant treatment alters MDM2 protein turnover and sensitivity of human breast carcinoma cells to chemotherapeutic drugs.Cancer letters · 2014Article
- Inhibition of RET increases the efficacy of antiestrogen and is a novel treatment strategy for luminal breast cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Significance of elevated ERK expression and its positive correlation with EGFR in Kazakh patients with esophageal squamous cell carcinoma.International journal of clinical and experimental pathology · 2014Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
Estrogen receptor-α (ER) targeted therapies are routinely used to treat breast cancer. However, patient responses are limited by resistance to endocrine therapy. Breast cancer cells resistant to the pure steroidal ER antagonist fulvestrant (fulv) demonstrate increased activation of epidermal growth factor receptor (EGFR) family members and downstream ERK signaling. In this study, we investigated the effects of fulv on EGFR signaling and ligand regulation in several breast cancer cell lines. EGFR/HER2/HER3 phosphorylation and ERK1,2 activation were seen after 24-48 h after fulvestrant treatment in ER-positive breast cancer cell lines. 4-Hydroxy-tamoxifen and estradiol did not cause EGFR activation. Fulvestrant did not affect EGFR expression. Cycloheximide abolished the ability of fulv to activate EGFR suggesting the autocrine production of EGFR ligands might be responsible for fulvestrant induced EGFR signaling. qRT-PCR results showed fulv differentially regulated EGFR ligands; HB-EGF mRNA was increased, while amphiregulin and epiregulin mRNAs were decreased. Fulvestrant induced EGFR activation and upregulation of EGFR ligands were ER dependent since fulv treatment in C4-12, an ER-negative cell line derivative of MCF-7 cells, did not result in EGFR activation or change in ligand mRNA levels. ER downregulation by siRNA induced similar EGFR activation and regulation of EGFR ligands as fulvestrant. Neutralizing HB-EGF antibody blocked fulv-induced EGFR activation. Combination of fulv and EGFR family tyrosine kinase inhibitors (erlotinib and lapatinib) significantly decreased EGFR signaling and cell survival. In conclusion, fulvestrant-activated EGFR family members accompanied by ER dependent upregulation of HB-EGF within 48 h. EGF receptor or ligand inhibition might enhance or prolong the therapeutic effects of targeting ER by fulvestrant in breast cancer.
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