The role of androgen receptor in breast cancer

Iacopetta, Domenico; Rechoum, Yassine; Fuqua, Suzanne A.W.

doi:10.1016/j.ddmec.2012.11.003

Cited by 54 publications

(44 citation statements)

References 95 publications

(100 reference statements)

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“…In breast cancer, the role of AR is complex because androgens can stimulate or inhibit cell growth [4, 7, 8, 18, 19, 22, 25, 28, 32]. Because of the dual actions of androgens in breast cancer, it is very important to identify biomarkers of AR activity to manage patients in AR-targeted studies, like the use of PSA monitoring in prostate cancer.…”

Section: Discussionmentioning

confidence: 99%

AR collaborates with ERα in aromatase inhibitor-resistant breast cancer

Rechoum

Rovito

Iacopetta

et al. 2014

Breast Cancer Res Treat

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108

104

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Androgen receptor (AR) is an attractive target in breast cancer because of its frequent expression in all the molecular subtypes, especially in estrogen receptor (ER)-positive luminal breast cancers. We have previously shown a role for AR overexpression in tamoxifen resistance. We engineered ER-positive MCF-7 cells to overexpress aromatase and AR (MCF-7 AR Arom cells) to explore the role of AR in aromatase inhibitor (AI) resistance. Androstendione (AD) was used as a substrate for aromatization to estrogen. The nonsteroidal AI anastrazole (Ana) inhibited AD-stimulated growth and ER transcriptional activity in MCF-7 Arom cells, but not in MCF-7 AR Arom cells. Enhanced activation of pIGF-1R and pAKT was found in AR-overexpressing cells, and their inhibitors restored sensitivity to Ana, suggesting that these pathways represent escape survival mechanisms. Sensitivity to Ana was restored with AR antagonists, or the antiestrogen fulvestrant. These results suggest that both AR and ERα must be blocked to restore sensitivity to hormonal therapies in AR-overexpressing ERα-positive breast cancers. AR contributed to ERα transcriptional activity in MCF-7 AR Arom cells, and AR and ERα co-localized in AD + Ana-treated cells, suggesting cooperation between the two receptors. AR-mediated resistance was associated with a failure to block ER transcriptional activity and enhanced up-regulation of AR and ER-responsive gene expression. Clinically, it may be necessary to block both AR and ERα in patients whose tumors express elevated levels of AR. In addition, inhibitors to the AKT/IGF-1R signaling pathways may provide alternative approaches to block escape pathways and restore hormone sensitivity in resistant breast tumors.

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Section: Discussionmentioning

confidence: 99%

AR collaborates with ERα in aromatase inhibitor-resistant breast cancer

Rechoum

Rovito

Iacopetta

et al. 2014

Breast Cancer Res Treat

Self Cite

108

104

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“…The AR is a well‐characterized clinical target in male prostate cancer, however, its diagnostic and therapeutic potential in female breast cancer has recently emerged in the literature. AR has clinical implications in both ER‐positive and ER‐negative breast tumors . In ER‐positive tumors, AR expression was associated with positive clinical outcomes.…”

Section: Hormone Signaling and Its Impact On Hcomentioning

confidence: 99%

Higher order genomic organization and epigenetic control maintain cellular identity and prevent breast cancer

Fritz

Gillis

Gerrard

et al. 2019

Genes Chromosomes & Cancer

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Cells establish and sustain structural and functional integrity of the genome to support cellular identity and prevent malignant transformation. In this review, we present a strategic overview of epigenetic regulatory mechanisms including histone modifications and higher order chromatin organization (HCO) that are perturbed in breast cancer onset and progression. Implications for dysfunctions that occur in hormone regulation, cell cycle control, and mitotic bookmarking in breast cancer are considered, with an emphasis on epithelial‐to‐mesenchymal transition and cancer stem cell activities. The architectural organization of regulatory machinery is addressed within the contexts of translating cancer‐compromised genomic organization to advances in breast cancer risk assessment, diagnosis, prognosis, and identification of novel therapeutic targets with high specificity and minimal off target effects.

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“…It has become clearer that thalidomide has multifaceted properties, leading many research groups to synthesize several derivatives and to study their effects, mostly in cancer research. The growth and progression of cancers require fundamental changes, for example, in energy metabolism pathways, nutrient uptake, and in several other factors, leading to phenotypic heterogeneity within subpopulations of cancer cells . These changes allow a greater capacity to grow under suboptimal micro‐environmental conditions such as nutrient depletion and hypoxia …”

Section: Introductionmentioning

confidence: 99%

Old Drug Scaffold, New Activity: Thalidomide‐Correlated Compounds Exert Different Effects on Breast Cancer Cell Growth and Progression

et al. 2017

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Thalidomide was first used for relief of morning sickness in pregnant women and then withdrawn from the market because of its dramatic effects on normal fetal development. Over the last decades, it has been used successfully for the treatment of several pathologies, including cancer. Many analogues with improved activity have been synthesized and tested. Herein we report some effects on the growth and progression of MCF-7 and MDA-MB-231 breast cancer cells by a small series of thalidomide-correlated compounds, which are very effective at inducing cancer cell death by triggering TNFα-mediated apoptosis. The most active compounds are able to drastically reduce the migration of breast cancer cells by regulation of the two major proteins involved in epithelial-mesenchymal transition (EMT): vimentin and E-cadherin. Moreover, these compounds diminish the intracellular biosynthesis of vascular endothelial growth factor (VEGF), which is primarily involved in the promotion of angiogenesis, sustaining tumor progression. The multiple features of these compounds that act on various key points of the tumorigenesis process make them good candidates for preclinical studies.

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The role of androgen receptor in breast cancer

Cited by 54 publications

References 95 publications

AR collaborates with ERα in aromatase inhibitor-resistant breast cancer

AR collaborates with ERα in aromatase inhibitor-resistant breast cancer

Higher order genomic organization and epigenetic control maintain cellular identity and prevent breast cancer

Old Drug Scaffold, New Activity: Thalidomide‐Correlated Compounds Exert Different Effects on Breast Cancer Cell Growth and Progression

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