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A mechanism of cooling hot tumors: lactate attenuates inflammation in dendritic cells [EGR1-KO]

ABSTRACT: We assessed the role of early growth response protein 1 (EGR1) in dendritic cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE163976 | GEO | 2021/08/23

REPOSITORIES: GEO

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A mechanism of cooling hot tumors: lactate attenuates inflammation in dendritic cells

Project description:The epigenetic status of H3K27Ac was comparable between Egr1 deficient and WT bone marrow-derived dendritic cells (BMDCs). We identified a region that suggested the interaction of EGR1 in the Cd80 promoter.

2021-08-23 | GSE164027 | GEO

A mechanism of cooling hot tumors: lactate attenuates inflammation in dendritic cells [EGR1-KO]

Project description:A mechanism of cooling hot tumors: lactate attenuates inflammation in dendritic cells [EGR1-KO]

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A mechanism of cooling hot tumors: lactate attenuates inflammation in dendritic cells [BMDCs]

Project description:Lactic acid (LA) accumulation in the tumour environment occurs as a result of the accelerated glucose metabolism in tumour cells, the so-called Warburg effect. Because TLR4 agonists are one of the damage-associated molecular patterns, which are important stimulators of dendritic cells in the tumour microenvironment, we assessed the effects of LA on the response to LPS, the TLR4 ligand.

2021-08-23 | GSE163975 | GEO

A mechanism of cooling hot tumors: Lactate attenuates inflammation in dendritic cells.

Project description:Turning non-inflamed (cold) tumors into inflamed (hot) tumors is important for maximizing the effect of immune checkpoint inhibitors (ICIs) against malignancies. We showed that lactate, a product of the Warburg effect, inhibited the efficacy of ICIs and suppressed IL-12 p40 expression in dendritic cells (DCs) through reducing NF-κB p65, p50, and c-Rel DNA-binding activity to the IL-12 p40 promoter. Additionally, lactate promoted the expression of early growth response protein 1 (EGR1), whose expression was increased in human invasive melanoma compared with non-invasive melanoma. We also found that EGR1 interacts with serum response factor (SRF) and represses the expression of CD80 in DCs. These findings suggest that lactate and its induced EGR1 are key factors that turn hot tumors into cold tumors and may represent targets in cancer treatment with ICIs.

| S-EPMC8441070 | biostudies-literature

A mechanism of cooling hot tumors: lactate attenuates inflammation in dendritic cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-08-23 | GSE163978 | GEO

A mechanism of cooling hot tumors: lactate attenuates inflammation in dendritic cells

Project description:A mechanism of cooling hot tumors: lactate attenuates inflammation in dendritic cells

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A mechanism of cooling hot tumors: lactate attenuates inflammation in dendritic cells

Project description:A mechanism of cooling hot tumors: lactate attenuates inflammation in dendritic cells

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A mechanism of cooling hot tumors: lactate attenuates inflammation in dendritic cells [BMDCs]

Project description:A mechanism of cooling hot tumors: lactate attenuates inflammation in dendritic cells [BMDCs]

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EGR1 regulation in human bone marrow stromal cells

Project description:Human bone marrow stromal cells (BMSCs) are key elements of the hematopoietic environment and they play a central role in bone and bone marrow physiology. However, how key BMSC functions are regulated is largely unknown. We analyzed the role of the immediate early response transcription factor EGR1 as key BMSC regulator and found that EGR1 was highly expressed in prospectively-isolated primary BMSCs, downregulated upon culture, and lower in non-CFU-F-containing CD45neg BM cells. Furthermore, EGR1 expression was lower in proliferative regenerating adult and fetal primary cells compared to adult steady-state BMSCs. Accordingly, EGR1 overexpression markedly decreased BMSC proliferation but considerably improved hematopoietic stroma support function as indicated by an increased production of transplantable CD34+CD90+ hematopoietic stem cells in expansion co-cultures. The improvement of BMSC stroma support function was mediated by increased expression of hematopoietic supporting genes, such as VCAM1 and CCL28. On the other hand, EGR1 knockdown increased ROS-mediated BMSC proliferation, and clearly reduced BMSC hematopoietic stroma support potential. These findings thus show that EGR1 is a key BMSC transcription factor with a dual role in regulating proliferation and hematopoietic stroma support function that is controlling a genetic program to coordinate the specific functions of BMSC in their different biological contexts.

2019-06-27 | PXD011767 | Pride

DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells

Project description:To gain insight into the function of DNA-PKcs within immune cells, we performed a quantitative phosphoproteomic screen in T cells to identify first order phosphorylation targets of DNA-PKcs. Results indicate that DNA-PKcs phosphorylates the transcription factor Egr1 (early growth response protein 1) at S301. Expression of Egr1 is induced early upon T cell activation and dictates T cell response by modulating expression of cytokines and key costimulatory molecules. Mutation of serine 301 to alanine via CRISPR-Cas9 resulted in increased proteasomal degradation of Egr1 and a decrease in Egr1-dependent transcription of IL2 (interleukin-2) in activated T cells. Our findings identify DNA-PKcs as a critical intermediary link between T cell activation and T cell fate and a novel phosphosite involved in regulating Egr1 activity.

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