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Transcriptomic analysis to uncover the mechanism of radiosensitization of AR-positive triple negative breast cancers with AR inhibition

ABSTRACT: Transcriptomic analysis to uncover the mechanism of radiosensitization of AR-positive triple negative breast cancers with AR inhibition

PROVIDER: PRJNA924670 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23096561_1.fastq.gz	Fastqsanger.gz
	SRR23096561_2.fastq.gz	Fastqsanger.gz
	SRR23096562_1.fastq.gz	Fastqsanger.gz
	SRR23096562_2.fastq.gz	Fastqsanger.gz
	SRR23096563_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis to uncover the mechanism of radiosensitization of AR-positive triple negative breast cancers with AR inhibition

Project description:We used charcoal-stripped serum on AR+ breast cancer cell lines to study the gene expression changes in the presence of androgens and/or radiation treatment in breast cancer.

2023-04-13 | GSE222992 | GEO

Effect of FOXA1 over-expression upon AR binding in AR-driven cancers

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Identification of a Therapeutically Targetable JAK-STAT Enriched Androgen Receptor (AR) and AR Splice Variant Positive Triple Negative Breast Cancer Subtype [project3]

Project description:Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with no targeted therapeutics. The luminal androgen receptor (LAR), one of the six TNBC subtypes, constitutes 15% of TNBC and is enriched for AR and AR-target genes. Here, we show that a cohort of TNBC not only expresses full-length AR (AR-FL) at a much higher rate (~80%) than previously reported, but also expresses AR splice variants (AR-SVs) (~20%), subclassifying the LAR-TNBC subtype into LAR-FL, LAR-AR-SV, or dual positive. Higher AR and AR-SV expression and corresponding aggressive phenotypes were observed predominantly in specimens obtained from African American women. RNA sequencing of LAR TNBC specimens indicates an enrichment of hallmark interferon, JAK-STAT, and androgen signaling pathways, which were exclusive to AR-expressing epithelial cancer cells as demonstrated by spatial genomics. LAR and LAR-AR-SV TNBC cell proliferation, orthotopic cell line and patient-derived xenograft, and patient-derived tumor explants growth were inhibited by AR N-terminal domain (NTD)-binding selective AR degrader (SARD) that irreversibly inhibits AR or by the JAK inhibitor ruxolitinib. Subsequent biochemical analysis suggests that STAT1 is an AR coactivator, and SARD or ruxolitinib blocks this coactivation. Collectively, our work identifies and characterizes a pharmacologically targetable and previously unreported TNBC subtype predominantly in African American women and identifies a growth-promoting interaction between AR and JAK-STAT signaling.

2023-10-04 | GSE244272 | GEO

Identification of a Therapeutically Targetable JAK-STAT Enriched Androgen Receptor (AR) and AR Splice Variant Positive Triple Negative Breast Cancer Subtype [project2]

2023-10-04 | GSE244271 | GEO

Identification of a Therapeutically Targetable JAK-STAT Enriched Androgen Receptor (AR) and AR Splice Variant Positive Triple Negative Breast Cancer Subtype [project4]

2023-10-04 | GSE244282 | GEO

Identification of a Therapeutically Targetable JAK-STAT Enriched Androgen Receptor (AR) and AR Splice Variant Positive Triple Negative Breast Cancer Subtype [Spacial]

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Characterization of the AR cistrome in ER-negative breast cancer cell lines

Project description:Although molecular apocrine and some triple negative breast cancer tumours express high levels of AR, how AR signalling impacts their proliferative rate remains an area of controversy. The precise molecular mechanisms by which the AR can induce divergent proliferative effects in estrogen receptor-negative breast cancers has not been described. The potent androgen, DHT, inhibits proliferation of the MFM-223 estrogen receptor-negative breast cancer cell line. In contrast, activation of the AR by DHT either stimulates, or has no effect, on MDA-MB-453 cell proliferation. The AR cistrome was examined in order to identify candidate factors which mediate oncogenic versus tumour suppressive AR activity in ER-negative breast cancer.

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Identification of a Therapeutically Targetable JAK-STAT Enriched Androgen Receptor (AR) and AR Splice Variant Positive Triple Negative Breast Cancer Subtype [MDA-MB-453]

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KIF15 promotes AR and AR-V7 protein stabilization in contribution to enzalutamide resistance of prostate cancers

Project description:KIF15 promotes AR and AR-V7 protein stabilization in contribution to enzalutamide resistance of prostate cancers

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Effect of FOXA1 over-expression upon AR binding in AR-driven cancers

Project description:We performed androgen receptor (AR) ChIP-seq after GFP control or FOXA1 over-expression in two AR driven cancer models; LNCaP prostate cancer cell line and MDA-MB-453 molecular apocrine breast cancer cell line.

2014-01-14 | E-MTAB-1749 | biostudies-arrayexpress

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