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Androgen Receptor is a Backdoor Inhibitor of Wildtype and Mutant Estrogen Receptors in Refractory Hormone Receptor-Positive Breast Cancers

ABSTRACT: Androgen Receptor is a Backdoor Inhibitor of Wildtype and Mutant Estrogen Receptors in Refractory Hormone Receptor-Positive Breast Cancers

PROVIDER: PRJNA526053 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8697940_1.fastq.gz	Fastqsanger.gz
	SRR8697940_2.fastq.gz	Fastqsanger.gz
	SRR8697950_1.fastq.gz	Fastqsanger.gz
	SRR8697950_2.fastq.gz	Fastqsanger.gz
	SRR8697931_1.fastq.gz	Fastqsanger.gz

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Androgen Receptor is a Backdoor Inhibitor of Wildtype and Mutant Estrogen Receptors in Refractory Hormone Receptor-Positive Breast Cancers

Project description:Ligand-activated AR inhibits wildtype and mutant-refractory ER activity in PDXs by reprogramming the ER and FOXA1 cistrome and rendering tumor-growth inhibition. These findings suggest that ligand-activated AR may function as a backdoor inhibitor of ER and that AR agonists may offer a safe and effective treatment for ER-positive breast cancer.

2019-09-19 | GSE128018 | GEO

Androgen receptor is a back-door inhibitor of Androgen Receptor is a Backdoor Inhibitor of Wildtype and Mutant Estrogen Receptors in Refractory Hormone Receptor-Positive Breast Cancers

Project description:Androgen receptor is a back-door inhibitor of Androgen Receptor is a Backdoor Inhibitor of Wildtype and Mutant Estrogen Receptors in Refractory Hormone Receptor-Positive Breast Cancers

| PRJNA521539 | ENA

Androgen receptor is a back-door inhibitor of Androgen Receptor is a Backdoor Inhibitor of Wildtype and Mutant Estrogen Receptors in Refractory Hormone Receptor-Positive Breast Cancers

Project description:HCI-13 patient-derived xenograft was treated with vehicle or a tissue-selective androgen receptor modulator (SARM), enobosarm. RNA was extracted from the tumors and microarray was performed. Objective: The objective of the study is to determine the effect of an androgen receptor (AR) agonist or a selective AR modulator (SARM) on hormone receptor-positive breast cancer growth in preclinical models and to determine the underlying mechanism of action.

2019-07-31 | GSE126318 | GEO

Androgen Receptor Is a Non-canonical Inhibitor of Wild-Type and Mutant Estrogen Receptors in Hormone Receptor-Positive Breast Cancers.

Project description:Sustained treatment of estrogen receptor (ER)-positive breast cancer with ER-targeting drugs results in ER mutations and refractory unresponsive cancers. Androgen receptor (AR), which is expressed in 80%-95% of ER-positive breast cancers, could serve as an alternate therapeutic target. Although AR agonists were used in the past to treat breast cancer, their use is currently infrequent due to virilizing side effects. Discovery of tissue-selective AR modulators (SARMs) has renewed interest in using AR agonists to treat breast cancer. Using translational models, we show that AR agonist and SARM, but not antagonist, inhibit the proliferation and growth of ER-positive breast cancer cells, patient-derived tissues, and patient-derived xenografts (PDX). Ligand-activated AR inhibits wild-type and mutant ER activity by reprogramming the ER and FOXA1 cistrome and rendering tumor growth inhibition. These findings suggest that ligand-activated AR may function as a non-canonical inhibitor of ER and that AR agonists may offer a safe and effective treatment for ER-positive breast cancer.

| S-EPMC6889594 | biostudies-literature

The androgen receptor in hormone-refractory prostate cancer.

Project description:Advanced prostate cancer is responsive to hormone therapy that interferes with androgen receptor (AR) signalling. However, the effect is short-lived, as nearly all tumours progress to a hormone-refractory (HR) state, a lethal stage of the disease. Intuitively, the AR should not be involved because hormone therapy that blocks or reduces AR activity is not effective in treating HR tumours. However, there is still a consensus that AR plays an essential role in HR prostate cancer (HRPC) because AR signalling is still functional in HR tumours. AR signalling can be activated in HR tumours through several mechanisms. First, activation of intracellular signal transduction pathways can sensitize the AR to castrate levels of androgens. Also, mutations in the AR can change AR ligand specificity, thereby allowing it to be activated by non-steroids or anti-androgens. Finally, overexpression of the wild-type AR sensitizes itself to low concentrations of androgens. Therefore, drugs targeting AR signalling could still be effective in treating HRPC.

| S-EPMC3735219 | biostudies-other

Refractory Cancers (RC) HOPE-CARE

Project description:Refractory Cancers (RC) HOPE-CARE

| PRJNA671240 | ENA

Transcription profiling of hormone sensitive and hormone refractory human prostate cancer xenografts grown in mice

Project description:Seven pairs of hormone sensitive and hormone refractory prostate cancer xenografts

2007-12-12 | E-GEOD-847 | biostudies-arrayexpress

Phosphorylation of the androgen receptor by PIM1 in hormone refractory prostate cancer.

Project description:Integration of cellular signaling pathways with androgen receptor (AR) signaling can be achieved through phosphorylation of AR by cellular kinases. However, the kinases responsible for phosphorylating the AR at numerous sites and the functional consequences of AR phosphorylation are only partially understood. Bioinformatic analysis revealed AR serine 213 (S213) as a putative substrate for PIM1, a kinase overexpressed in prostate cancer. Therefore, phosphorylation of AR serine 213 by PIM1 was examined using a phosphorylation site-specific antibody. Wild-type PIM1, but not catalytically inactive PIM1, specifically phosphorylated AR but not an AR serine-to-alanine mutant (S213A). In vitro kinase assays confirmed that PIM1 can phosphorylate AR S213 in a ligand-independent manner and cell type-specific phosphorylation was observed in prostate cancer cell lines. Upon PIM1 overexpression, AR phosphorylation was observed in the absence of hormone and was further increased in the presence of hormone in LNCaP, LNCaP-abl and VCaP cells. Moreover, phosphorylation of AR was reduced in the presence of PIM kinase inhibitors. An examination of AR-mediated transcription showed that reporter gene activity was reduced in the presence of PIM1 and wild-type AR, but not S213A mutant AR. Androgen-mediated transcription of endogenous PSA, Nkx3.1 and IGFBP5 was also decreased in the presence of PIM1, whereas IL6, cyclin A1 and caveolin 2 were increased. Immunohistochemical analysis of prostate cancer tissue microarrays showed significant P-AR S213 expression that was associated with hormone refractory prostate cancers, likely identifying cells with catalytically active PIM1. In addition, prostate cancers expressing a high level of P-AR S213 were twice as likely to be from biochemically recurrent cancers. Thus, AR phosphorylation by PIM1 at S213 impacts gene transcription and is highly prevalent in aggressive prostate cancer.

| S-EPMC3527659 | biostudies-literature

Estrogen receptors in breast cancer stem cells

Project description:Breast cancer stem cells are considered estrogen receptor negative and estrogen insensitive. However, estrogens potentiate growth of the vast majority of breast tumors. In this study, we characterize the expression of estrogen receptors in breast cancer stem cells. We used microarrays to characterize the global gene expression underlying estrogen receptor activation versus inhibition in breast cancer cells from invasive breast cancers. Cancer cells from invasive breast carcinomas are treated with D (DPN), T (4OHT) or untreated (vehicle control).

2012-01-12 | E-GEOD-35031 | biostudies-arrayexpress

Effects of WCE herbal extract on hormone-refractory PC-3 tumors

Project description:Purpose: Androgen-deprivation therapy is the standard treatment for prostate cancer but fails in hormone-refractory prostate cancer. The anti-inflammatory plant Wedelia chinensis is rich in luteolin, apigenin, and wedelolactone that act synergistically to suppress androgen receptor activity in prostate cancer. Here, we evaluated the systemic antitumor effects of a standardized and effect-optimized Wedelia chinensis herbal extract (WCE) on hormone-refractory prostate cancer. Methods: Hormone-refractory PC-3 orthotopic tumor mouse models were orally administered with WCE. The tumor transcriptomes were studied using RNA sequencing and Ingenuity Pathway Analysis to identify the molecular mechanisms. Results: WCE significantly attenuated tumor growth and metastasis in orthotopic PC-3 xenografts. Transcriptomic analysis of genome-wide gene expression in the tumors revealed that WCE suppressed the expression of HIF1α, IKKα/β phosphorylation, and the downstream cytokines/chemokines. Conclusions: A standardized preparation of Wedelia chinensis improved prostate cancer therapy through repressing NFκB-mediated cytokine expression in tumor cells and modulating the inflammatory tumor microenvironment. These data suggest that WCE functions through immunomodulation and has potential application as an adjuvant agent for the treatment of castration-resistant prostate cancer.

2017-12-01 | GSE99820 | GEO

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