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Prolonged estrogen deprivation triggers a broad immunosuppressive phenotype in breast cancer cells

ABSTRACT: Prolonged estrogen deprivation triggers a broad immunosuppressive phenotype in breast cancer cells

PROVIDER: PRJNA753846 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15417454_1.fastq.gz	Fastqsanger.gz
	SRR15417454_2.fastq.gz	Fastqsanger.gz
	SRR15417455_1.fastq.gz	Fastqsanger.gz
	SRR15417455_2.fastq.gz	Fastqsanger.gz
	SRR15417456_1.fastq.gz	Fastqsanger.gz

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Estrogen deprivation triggers and immunosuppressive phenotype in breast cancer cells

Project description:Estrogen deprivation triggers and immunosuppressive phenotype in breast cancer cells

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Prolonged estrogen deprivation triggers a broad immunosuppressive phenotype in breast cancer cells.

Project description:Among others, expression levels of programmed cell death 1 ligand 1 (PD-L1) have been explored as biomarkers of the response to immune checkpoint inhibitors in cancer therapy. Here, we present the results of a chemical screen that interrogated how medically approved drugs influence PD-L1 expression. As expected, corticosteroids and inhibitors of Janus kinases were among the top PD-L1 downregulators. In addition, we identified that PD-L1 expression is induced by antiestrogenic compounds. Transcriptomic analyses indicate that chronic estrogen receptor alpha (ERα) inhibition triggers a broad immunosuppressive program in ER-positive breast cancer cells, which is subsequent to their growth arrest and involves the activation of multiple immune checkpoints together with the silencing of the antigen-presenting machinery. Accordingly, estrogen-deprived MCF7 cells are resistant to T-cell-mediated cell killing, in a manner that is independent of PD-L1, but which is reverted by estradiol. Our study reveals that while antiestrogen therapies efficiently limit the growth of ER-positive breast cancer cells, they concomitantly trigger a transcriptional program that favors their immune evasion.

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Prolonged estrogen deprivation triggers a broad immunosuppressive phenotype in breast cancer cells

Project description:Our study reveals that while antiestrogen therapies effectively limit tumor growth in ER-positive breast cancers, they also trigger a transcriptional program that favors immune evasion.

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Prolonged sleep deprivation induces cytokine storm-like syndrome in mammals

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Prolonged sleep deprivation induces cytokine storm-like syndrome in mammals [scRNA-Seq]

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Project description:Prolonged sleep deprivation induces cytokine storm-like syndrome in mammals

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Prolonged sleep deprivation induces cytokine storm-like syndrome in mammals [scRNA-Seq]

Project description:Prolonged sleep deprivation induces cytokine storm-like syndrome in mammals [scRNA-Seq]

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Prolonged sleep deprivation induces cytokine storm-like syndrome in mammals [RNA-Seq]

Project description:Prolonged sleep deprivation induces cytokine storm-like syndrome in mammals [RNA-Seq]

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HIV-1 Vpu exerts broad immunosuppressive effects by inhibiting NF-κB-dependent gene expression

Project description:Using an unbiased RNA sequencing approach of primary CD4+ T cells infected with three wild type primary HIV-1 isolates and selective mutants thereof, Langer et al. show that the HIV-1 accessory protein Vpu exerts broad immunosuppressive effects, inhibiting the induction of innate and adaptive immune responses. Transcription factor network analyses reveal that Vpu suppresses the expression of NF‑κB rather than IRF3 target genes. As a result, Vpu impairs the production of pro-inflammatory cytokines such as IFNβ, CXCL10 and IL-6.

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