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Spatial transcriptomics reveals functional compartmentalization of estrogen receptor positive (ER+) breast cancer

ABSTRACT: Spatial transcriptomics reveals functional compartmentalization of estrogen receptor positive (ER+) breast cancer

PROVIDER: PRJNA885881 | ENA |

REPOSITORIES: ENA

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Spatial transcriptomics reveals functional compartmentalization of estrogen receptor positive (ER+) breast cancer

Project description:Intratumor heterogeneity is one of the hallmarks of cancers, including breast cancers. We performed spatial transcriptomics to profile heterogeneous cell populations within ER+ breast cancers as well as to determine their importance for estrogen-dependent tumor growth. Our analysis has revealed the key functional compartments for developing targeted therapeutic strategies against ER+ breast cancers.

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Characterization of estrogen regulation in estrogen reseptor (ER)-positive breast cancer at the single cell level

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Transcription profiling of mouse normal mammary gland epithelial populations: basal/myoepithelial, luminal estrogen receptor negative (ER-) and luminal estrogen receptor positive (ER+) cells

Project description:The goal of the experiment was to carry out a transcriptome analysis of the three main epithelial cell populations of the mouse mammary gland, the basal/myoepithelial, luminal estrogen receptor negative (ER-) and luminal estrogen receptor positive (ER+) cells, to identify cell-type specific differences in gene expression. Three replicates arrays were carried out for each of the three populations (a total of nine arrays). Each replicate was a genuine biological replicate from RNA harvested from completely independent cell preparations. Each sample was isolated from preparations of mammary epithelium derived fourth mammary fat pads of 8 * 10 week old virgin female FVB mice. Each preparation was from a pool of 10 * 20 animals (20 * 40 fat pads).

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Project description:Hormone therapy targeting estrogen receptor (ER) is the principal treatment for ER-positive breast cancers but many cancers develop resistance to anti-estrogens. Cyclin-dependent kinase 8 (CDK8) is a transcriptional regulator of several oncogenic pathways. Expression levels of CDK8 and ERα are inversely correlated in breast cancers suggesting a functional association between CDK8 and ER. CDK8 inhibition by selective small-molecule inhibitors, by shRNA knockdown or by CRISPR-Cas9 knockout suppressed estrogen-induced transcription, with no significant effects on ERα protein expression or phosphorylation. CDK8 inhibition also abrogated the mitogenic effect of estrogen on ER-positive breast cancer cells and potentiated growth inhibition by the ER antagonist fulvestrant. In vivo, administration of a CDK8 inhibitor suppressed ER-positive breast cancer xenograft growth and augmented the effects of fulvestrant with no apparent toxicity. CDK8 inhibitors also suppressed the development of estrogen independence in ER-positive breast cancer cells. These results identify CDK8 as a novel drug target for breast cancer therapy.

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Estrogen Receptor Positive Breast Cancer: Aromatase Inhibitor Response Study

Project description:<p>Highly variable outcomes are observed in patients with estrogen receptor positive (ER+) breast cancer who undergo preoperative estrogen deprivation therapy with aromatase inhibitors (AI). In this study, 46 baseline tumor and normal genomes and 31 baseline tumor/normal exomes of participants selected from two clinical trials of neoadjuvant AI therapy on ER+ breast cancer were sequenced to identify somatic alterations that correlate with response to AI, to screen for therapeutic targets and to elucidate the genetic landscape of ER+ breast cancer. From the same set of patients we later performed deep genomic characterization of a subset of matched primary tumors after four months of AI therapy, generating comprehensive information about the range of changes that occur when ER+ breast cancers are subjected to estrogen deprivation. This data includes whole genome sequence and transcriptome data. To better understand tumor heterogeneity and the evolution of resistance to estrogen-deprivation therapy, a subset of these tumours, along with 38 additional cases were sequenced to greater depth using targeted capture with a gene panel.</p>

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microRNA expression signature in estrogen receptor-positive and -negative breast cancers

Project description:Micro RNA (miRNA) profiling of breast cancer subtype was demonstrated using RT-PCR. We present herein two cases with miRNA profiling in estrogen receptor (ER)-positive and -negative breast cancer. The level of miR-181a expression in ER-positive cancer was higher than in ER-negative cancer, while expression of miR-27a, -107 and -195 was lower in ER-positive when compared with ER-negative cancer.

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Project description:HNRNPAB interacted with mRNAs in estrogen receptor positive (ER+) breast cancer [RIP-Seq]

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CircESR1 and HNRNPAB function in estrogen receptor positive (ER+) breast cancer [RNA-Seq]

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Estrogen-induced CircRNA, CircPGR, Functions as a CeRNA to Promote Estrogen Receptor-positive Breast Cancer Progression by Regulating Cell Cycle-related Genes

Project description:Estrogen and estrogen receptor (ER)-mediated gene transcriptional events have been well known to be involved in ER-positive breast carcinogenesis. Meanwhile, circular RNAs (circRNAs) are emerging as a new family of functional non-coding RNAs (ncRNAs) with implications in a variety of pathological processes, such as cancer. However, the estrogen-regulated circRNA program and the function of such program remain uncharacterized. Here, genome-wide circRNA profiling by circRNA sequencing (circRNA-seq) revealed tens of thousands of circRNAs were induced by estrogen, and further functional screening for the several circRNAs originated from PGR revealed that one of them, which we named as circPGR, was required for ER-positive breast cancer cell growth and tumorigenesis. CircPGR was found to be localized in the cytosol of cells. Mechanistically, circPGR functioned as a competing endogenous RNA (ceRNA) to sponge miR-301a-5p to regulate the expression of multiple cell cycle genes. The clinical relevance of circPGR was underscored by its high and specific expression in ER-positive breast cancer cell lines and clinical breast cancer tissue samples. Accordingly, siRNA targeting circPGR was proven to be effective in suppressing ER-positive breast cancer cell growth. These findings reveled that, besides the well-known mRNA, microRNA (miRNA), long non-coding RNA (lncRNA) and enhancer RNA (eRNA) programs, estrogen also induced a circRNA program, and exemplified by circPGR, these estrogen-induced circRNAs were required for ER-positive breast cancer cell growth, providing a new class of therapeutic targets for ER-positive breast cancer.

2023-02-13 | GSE145729 | GEO

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