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Transcriptome of juvenile zebrafish treated with the aromatase inhibitor exemestane and solvent control

ABSTRACT: Transcriptome of juvenile zebrafish treated with the aromatase inhibitor exemestane and solvent control

PROVIDER: PRJNA596870 | ENA |

REPOSITORIES: ENA

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Transcriptome of juvenile zebrafish treated with the aromatase inhibitor exemestane and solvent control

Project description:To reveal the transcriptomic changes during the sex differetiation in larval zebrafish, we treated the lavarl fish with aromatase inhibitors (EM, CAS: 107868-30-4, 100 μg/L), as well as solvent as a control, and sampled them after the exposure.

2019-12-20 | GSE142353 | GEO

mRNA-seq of gonads from adult zebrafish treated with aromatase inhibitor and control

Project description:To explore the transcriptional effects of aromatase inhibitors on sex differentiation of zebrafish, we exposed 3-month-old zebrafish (AB strain) to the third generation aromatase inhibitor Exemestane (CAS: 107868-30-4) and characterized transcript abundance among testes and ovaries after 32 days of drug exposure. After the drug treatment, we dissected zebrafish gonads, isolated polyA+ RNA and performed high-throughput RNA-Seq analysis.

2019-12-07 | GSE123439 | GEO

mRNA-seq of zebrafish treated with sex hormone 17β-estradiol and aromatase inhibitor exemestane during sex development

Project description:To identify key genes in the early sex development of zebrafish, we generated zebrafish (AB strain) feminized by sex hormone 17β-estradiol (E2, CAS: 50-28-2, 100 ng/L) and masculinized by aromatase inhibitor exemestane (EM, CAS: 107868-30-4, 10 μg/L), and detected their transcriptomes by RNA-seq.

2022-05-11 | GSE126039 | GEO

Expression data from MCF-7aro aromatase inhibitor-resistant, tamoxifen-resistant and LTEDaro lines.

2008-03-22 | GSE10911 | GEO

Transcription profiling of human cell lines resistant to aromatase inhibitor, tamoxifen-resistant and LTEDaro lines

Project description:MCF-7aro cells were used to generate a cell culture model system that is resistant to 3 aromatase inhibitors (AIs), letrozole, anastrozole and exemestane. For comparison, the MCF-7aro cells were also used to generate the tamoxifen-resistant cells as well as long-term estrogen deprived, LTEDaro. Affymetrix microarray analysis was performed to determine changes in gene expression that are unique to AI-resistance. Experiment Overall Design: For control purposes, MCF-7aro cells were cultured without any hormone or inhibitor as well as a hormone-only control (T-only). Resistant cells were grown in the presence of testosterone, T+LET R (letrozole), T+ANA R (anastrozole), T+EXE R (exemestane), T+TAM R (Tamoxifen). In addition, testosterone-free resistant lines were generated, LTEDaro, ANA R and EXE R. 6 replicates were generated for the hormone-containing resistant lines and 3 replicates for the hormone-free resistant lines.

2008-04-04 | E-GEOD-10911 | biostudies-arrayexpress

Antitumor Activity of Z-endoxifen in Aromatase Inhibitor-Sensitive and Resistant Estrogen Receptor-Positive Breast Cancer

Project description:The overarching goal of this study was to explore the antitumor activity of Z-endoxifen, a tamoxifen metabolite, with first-line endocrine therapies tamoxifen and letrozole in the letrozole-sensitive MCF7 aromatase expressing model (MCF7AC1), and with second-line endocrine therapies including tamoxifen, fulvestrant, exemestane, and exemestane plus everolimus, in letrozole-resistant MCF7 model (MCF7LR) in vivo. We used microarray to identify genes that are commonly and differently reguated by Z-endoxifen and tamoxifen treatments in the letrozole-resistant MCF7LR tumors.

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The gene expression of aromatase-inhibitor-resistant cell line

2014-04-01 | GSE51390 | GEO

The gene expression of aromatase-inhibitor-resistant cell line

Project description:To identify the genes which have relation to aromatase-inhibitor-resistance, we compared the gene expression of aromatase-inhibitor-resistant cell, A3, with that of parent cell line, T-47D. Because A3 showed remarkable cell proliferation by 1nM Dihydrotestosterone(DHT), cells were cultured with DHTand bicalutamide for 24h, and total RNA was extracted.

2014-04-01 | E-GEOD-51390 | biostudies-arrayexpress

mRNA-seq of zebrafish treated with sex hormone 17β-estradiol and aromatase inhibitor exemestane during sex development

Project description:mRNA-seq of zebrafish treated with sex hormone 17β-estradiol and aromatase inhibitor exemestane during sex development

| PRJNA520845 | ENA

GDNF-RET signaling as a target in aromatase inhibitor resistant breast cancers

Project description:Understanding the complex molecular mechanisms underlying resistance to endocrine therapy is a major challenge in the treatment of estrogen receptor-positive (ER+) breast cancers. We have previously demonstrated that glial cell line-derived neurotrophic factor (GDNF) signaling via the receptor tyrosine kinase RET promotes estrogen independent activation of ER. Here we have addressed the relevance of GDNF-RET signaling in response to aromatase inhibitor treatment and explored the efficacy of using RET inhibitors in breast cancer models of aromatase inhibitor response and resistance. A GDNF-response gene set, identified from gene expression profiling, was demonstrated to be an independent prognostic marker of poor patient outcome and, importantly, to be predictive of poor response to aromatase inhibitor treatment and development of resistance. The relevance of these findings was validated first by demonstrating an association of RET protein expression in an independent cohort of aromatase inhibitor resistant patient samples. Second, in in vitro models, GDNF-mediated RET signaling was demonstrated to enhance the survival of aromatase inhibitor resistant cells and to increase resistance in aromatase inhibitor sensitive cells. These effects could be reversed by targeting GDNF/RET signaling with the RET selective inhibitor NVP-BBT594 thus identifying GDNF-RET signaling as a potential therapeutic target, particularly in breast cancers resistant to aromatase inhibitors.<br>MCF7 cells were E2-deprived by culturing in phenol red-free RPMI 1640 supplemented with 10% DCC for 3 days and then serum-starved overnight in the presence or absence of fulvestrant (ICI182,780) (100 nM). The following day, cells were treated with GDNF (20 ng/ml) for 0, 4, 8, 24 and 48 hours in the presence or absence of fulvestrant (ICI182,780) (100 nM).

2013-01-17 | E-MEXP-3662 | biostudies-arrayexpress

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