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Spermine-induced gene expression change in human macrophages

ABSTRACT: Polyamines, crucial molecules involved in cell proliferation and growth, play a pivotal role in cancer development and progression. Within the tumor microenvironment, macrophages, key components of the immune system, exhibit a complex relationship with polyamines. Evidence suggests that polyamines can modulate macrophage polarization, influencing their functional phenotypes. Here, we detected the gene expression changes in spermine-stimulated human macrophages isolated from PBMCs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE266867 | GEO | 2024/05/12

REPOSITORIES: GEO

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Spermine-induced DNA methylation change in human macrophages

Project description:Polyamines, crucial molecules involved in cell proliferation and growth, play a pivotal role in cancer development and progression. Within the tumor microenvironment, macrophages, key components of the immune system, exhibit a complex relationship with polyamines. Evidence suggests that polyamines can modulate macrophage polarization, influencing their functional phenotypes. Here, we detected the gene DNA methylation changes in spermine-stimulated human macrophages isolated from PBMCs and TAMs.

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Spermine-induced gene expression change in human macrophages

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Tpo1‐mediated spermine and spermidine export controls cell cycle delay and times antioxidant protein expression during the oxidative stress response

Project description:Cells counteract oxidative stress by altering metabolism, cell cycle and gene expression. However, the mechanisms that coordinate these adaptations are only marginally understood. Here we provide evidence that timing of these responses in yeast requires export of the polyamines spermidine and spermine. We show that during hydrogen peroxide (H2O2) exposure, the polyamine transporter Tpo1 controls spermidine and spermine concentrations and mediates induction of antioxidant proteins, including Hsp70, Hsp90, Hsp104 and Sod1. Moreover, Tpo1 determines a cell cycle delay during adaptation to increased oxidant levels, and affects H2O2 tolerance. Thus, central components of the stress response are timed through Tpo1‐controlled polyamine export.

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