ArticleOncotarget2017
Estrogen receptor β2 induces proliferation and invasiveness of triple negative breast cancer cells: association with regulation of PHD3 and HIF-1α.
Article in Oncotarget, 2017. 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, 25 citations in OpenAlex.
- Association of Nuclear Receptor Coactivators with Hypoxia-Inducible Factor-1BioMed research international · 2020Trial
- ERβ in Granulosa Cell Tumors and Its Clinical Potential.Endocrinology · 2023Review
- ERβ1 Sensitizes and ERβ2 Desensitizes ERα-Positive Breast Cancer Cells to the Inhibitory Effects of Tamoxifen, Fulvestrant and Their Combination with All-Trans Retinoic Acid.International journal of molecular sciences · 2023Article
- Divergent features of ERβ isoforms in triple negative breast cancer: progress and implications for further research.Frontiers in cell and developmental biology · 2023Review
- The Role of Hypoxia-Inducible Factor Isoforms in Breast Cancer and Perspectives on Their Inhibition in Therapy.Cancers · 2022Review
- Estrogen receptor β2 (ERβ2)-mediated upregulation of hsa_circ_0000732 promotes tumor progression via sponging microRNA-1184 in triple-negative breast cancer (TNBC).Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Estrogen Receptors-Mediated Apoptosis in Hormone-Dependent Cancers.International journal of molecular sciences · 2022Review
- Multifaceted Interplay between Hormones, Growth Factors and Hypoxia in the Tumor Microenvironment.Cancers · 2022Review
- Article
- Contrasting activities of estrogen receptor beta isoforms in triple negative breast cancer.Breast cancer research and treatment · 2021Article
- Estrogen Receptor Beta (ERβ): A Ligand Activated Tumor Suppressor.Frontiers in oncology · 2020Review
- Estrogen receptor-beta is a potential target for triple negative breast cancer treatment.Oncotarget · 2018Article
- Duality of estrogen receptor β action in cancer progression.Current opinion in pharmacology · 2018Review
- Crosstalk between Notch, HIF-1α and GPER in Breast Cancer EMT.International journal of molecular sciences · 2018Review
- Mechanisms for estrogen receptor expression in human cancer.Experimental hematology & oncology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The two estrogen receptor (ER) subtypes, ERα and ERβ, belong to the nuclear receptor superfamily. The human ERβ variant ERβ2 is proposed to be expressed at higher levels than ERβ1 in many breast tumors and it has been suggested that ERβ2, in contrast to ERβ1, is associated with aggressive phenotypes of various cancers. However, the role of endogenous ERβ2 in breast cancer cells remains elusive. In this study, we identified that triple negative breast cancer (TNBC) cell lines express endogenous ERβ2, but not ERα or ERβ1. This allows novel studies of endogenous ERβ2 functions independent of ERα and ERβ1. We show that overexpression of ERβ2 in TNBC cells increased whereas knockdown of endogenous ERβ2 decreased cell proliferation and cell invasion. To elucidate the molecular mechanism responsible for these cellular phenotypes, we assayed ERβ2 dependent global gene expression profiles. We show that ERβ2 decreases prolyl hydroxylase 3 (PHD3) gene expression and further show that this is associated with increased hypoxia inducible factor 1α (HIF-1α) protein levels, thus providing a possible mechanism for the invasive phenotype. These results are further supported by analysing the expression of ERβ2 and PHD3 in breast tumor samples where a negative correlation between ERβ2 and PHD3 expression was observed. Together, we demonstrate that ERβ2 has an important role in enhancing cell proliferation and invasion, beyond modulation of ERβ and ERβ1 signalling which might contribute to the invasive characteristics of TNBC. The invasive phenotype could potentially be mediated through transcriptional repression of PHD3 and increased HIF-1α protein levels.
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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.