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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.

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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 [project4]

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 | GSE244282 | GEO

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

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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 [project2]

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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 [Spacial]

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

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

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ABI1 regulates transcriptional activity of Androgen Receptor by novel DNA and AR binding mechanism [ChIP-seq]

Project description:Transcription regulates key functions of living organisms in normal and disease states, including cell growth and development, embryonic and adult tissue organization, and tumor progression. Here we identify a novel mechanism of transcriptional regulation by an actin regulatory and signaling protein, Abelson Interactor 1(ABI1). Using prostate cancer models, we uncover a reciprocal regulation between ABI1 and the Androgen Receptor (AR). ABI1 is a direct, androgen-regulated target; in turn, ABI1 interacts with AR and its splice variant ARv7, and co-regulates a subset of specific transcriptional targets. ABI1 directs transcription through transient yet well-defined interaction of its intrinsically disordered region with DNA. Clinical evaluation shows that both the ABI1-DNA binding (through Exon 4 splicing) and ABI1-AR interaction are regulated during androgen deprivation therapy and prostate cancer progression, thus controlling tumor plasticity through connecting actin cytoskeleton and cellular signaling to transcriptional regulation. We propose that ABI1 is an epigenetic regulator of transcriptional homeostasis in AR-driven cancers.

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ABI1 regulates transcriptional activity of Androgen Receptor by novel DNA and AR binding mechanism [RNA-seq]

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