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Homo sapiens

ABSTRACT: RNA-seq in two ER+ breast cancer cell lines with and without progestins

OTHER RELATED OMICS DATASETS IN: PXD002104

PROVIDER: PRJNA282505 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2001020.fastq.gz	Fastqsanger.gz
	SRR2001030.fastq.gz	Fastqsanger.gz
	SRR2001040.fastq.gz	Fastqsanger.gz
	SRR2001050.fastq.gz	Fastqsanger.gz
	SRR2001060.fastq.gz	Fastqsanger.gz

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Project description:Obesity is a known risk factor for breast cancer. To identify genes and underlying pathways in human breast cancer cells affected by interaction with mature adipocytes, two estrogen-receptor positive (ER+) breast cancer cell lines, MCF-7 and T47D, and the triple-negative (TN) breast cancer cell line MDA-MB-231 were cultivated in a co-culture system with or without differentiated murine 3T3-L1 adipocytes for the purpose of a microarray gene expression analysis. The use of in vitro differentiated 3T3-L1 adipocytes allowed comparable experimental conditions for each of the co-culture experiments with human breast cancer cell lines. For co-cultivation analyses of 3T3-L1 and breast cancer cells, we set up a two-dimensional transwell system, which enables intercellular communication through soluble factors secreted into the medium but inhibits intermixture of the different cell types. Following 5 days of co-culture with or without differentiated adipocytes, total RNA was isolated from the human breast cancer cells and subjected to microarray gene expression analyses.

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Profiling of three different ER+ breast cancer cell lines grown in the presence and absence of estrogen.

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Project description:Hormonal contraception exposes women to different synthetic progesterone receptor (PR) agonists, progestins, and transiently increases breast cancer risk. How progestins affect the breast epithelium is poorly understood because we lack adequate models to study this. We hypothesized that individual progestins differentially affect cell proliferation in the normal breast epithelium and hence breast cancer risk. Using mouse mammary tissue ex vivo, we show that testosterone-related progestins strongly induce the PR target and mediator of PR signaling induced cell proliferation Receptor Activator of NF-κB Ligand (Rankl), previously implicated in breast carcinogenesis, whereas other progestins fail to do so. We developed xenografts of normal human breast epithelial cells (HBECSs) to the milk ducts of immunocompromised female mice and show that they remain hormone-responsive. Using HBECSs from 36 women, we show that testosterone-related progestins, desogestrel, gestodene, and levonorgestrel, induce PSA (KLK3) and promote their proliferation, whereas the anti-androgenic progestins, which have shown anti-androgenic properties in reporter assays, chlormadinone acetate and cyproterone acetate, do not. Pharmacological inhibition of the androgen receptor (AR) inhibits PR agonist and levonorgestrel-induced RANKL expression and both pharmacological and genetic AR inhibition reduce levonorgestrel-driven breast epithelial cell proliferation in vivo. Prolonged exposure to androgenic progestins elicits hyperproliferation with cytologic changes. Thus, different progestins have distinct biological activities in the breast epithelium that should be taken into account for more informed choices in hormonal contraception.

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Xenografted breast epithelia reveal differences in growth stimulation among contraceptive progestins related to androgenic properties [human]

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2022-02-16 | PXD028537 | Pride

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