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Tumor-associated macrophages respond to chemotherapy by detrimental transcriptional reprogramming and suppressing stabilin-1 mediated clearance of EGF

ABSTRACT: Tumor-associated macrophages respond to chemotherapy by detrimental transcriptional reprogramming and suppressing stabilin-1 mediated clearance of EGF

PROVIDER: PRJNA932034 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23353516.fastq.gz	Fastqsanger.gz
	SRR23353517.fastq.gz	Fastqsanger.gz
	SRR23353518.fastq.gz	Fastqsanger.gz
	SRR23353519.fastq.gz	Fastqsanger.gz
	SRR23353520.fastq.gz	Fastqsanger.gz

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Tumor-associated macrophages respond to chemotherapy by detrimental transcriptional reprogramming and suppressing stabilin-1 mediated clearance of EGF

Project description:Tumor resistance to chemotherapy and metastatic relapse account for more than 90% of cancer specific mortality. Tumor associated macrophages (TAMs) can process chemotherapeutic agents and impair their action. Little is known about the direct effects of chemotherapy on TAMs. Here we show that chemotherapeutic agent cisplatin can initiate detrimental transcriptional and functional programs in TAMs, without significant impairment of their viability. We focused on the clearance function of TAMs that controls composition of tumor microenvironment. For the first time we demonstrated, that TAMs scavenger receptor stabilin-1 is responsible for the clearance of EGF, a potent stimulator of tumor growth. Cisplatin suppressed both overall and EGF-specific endocytosis in TAMs by bidirectional mode: suppression of positive regulators and stimulation of negative regulators of endocytosis, with strongest effect on SYT11, confirmed in patients with breast cancer. Our data demonstrate that synergistic action of cytostatic agents and innovative immunomodulators is required to overcome cancer therapy resistance.

2023-02-10 | GSE224681 | GEO

Tumor-associated macrophages respond to chemotherapy by detrimental transcriptional reprogramming and suppressing stabilin-1 mediated clearance of EGF.

Project description:IntroductionTumor resistance to chemotherapy and metastatic relapse account for more than 90% of cancer specific mortality. Tumor-associated macrophages (TAMs) can process chemotherapeutic agents and impair their action. Little is known about the direct effects of chemotherapy on TAMs.MethodsThe effect of chemotherapeutic platinum agent cisplatin was assessed in the model system of human ex vivo TAMs. Whole-transcriptome sequencing for paired TAMs stimulated and not stimulated by cisplatin was analysed by NGS. Endocytic uptake of EGF was quantified by flow cytometry. Confocal microscopy was used to visualize stabilin-1-mediated internalization and endocytic trafficking of EGF in CHO cells expressing ectopically recombinant stabilin-1 and in stabilin-1+ TAMs. In cohort of patients with breast cancer, the effect of platinum therapy on the transcriptome of TAMs was validated, and differential expression of regulators of endocytosis was identified.ResultsHere we show that chemotherapeutic agent cisplatin can initiate detrimental transcriptional and functional programs in TAMs, without significant impairment of their viability. We focused on the clearance function of TAMs that controls composition of tumor microenvironment. For the first time we demonstrated that TAMs' scavenger receptor stabilin-1 is responsible for the clearance of epidermal growth factor (EGF), a potent stimulator of tumor growth. Cisplatin suppressed both overall and EGF-specific endocytosis in TAMs by bidirectional mode: suppression of positive regulators and stimulation of negative regulators of endocytosis, with strongest effect on synaptotagmin-11 (SYT11), confirmed in patients with breast cancer.ConclusionOur data demonstrate that synergistic action of cytostatic agents and innovative immunomodulators is required to overcome cancer therapy resistance.

| S-EPMC10028613 | biostudies-literature

Methotrexate Clearance

Project description:Methotrexate Clearance

| PRJNA76037 | ENA

Beneficial and detrimental consequences of AHR stimulation in intestinal infection

Project description:The ligand dependent transcription factor aryl hydrocarbon receptor (AHR) is an environmental sensor whose activation can have physiologically beneficial or detrimental consequences for host immune responses depending on the ligand. Here we investigated the hypothesis that prolonged AHR activation either due to inefficient ligand metabolism or due to genetic manipulation may underlie the distinction between beneficial and detrimental effects. Our data indicate that prolonged AHR activation caused toxic endpoints for liver and thymus but was not per se interfering with the host response to infection with the intestinal pathogen C.rodentium. Genetically driven constitutive AHR activation improved resistance to infection, whereas prolonged AHR activation by the pollutant TCDD resulted in delayed clearance of C.rodentium. This was associated to a suppression in antibody production. Combined single cell RNAseq and ATAC-seq analysis provided evidence that TCDD, but not genetic AHR overactivation, affected dendritic cell functions such as activation, maturation and antigen presentation. Thus, the detrimental impact of environmental pollutants such as TCDD on immune responses cannot solely be attributed to aberrantly prolonged activation of AHR.

2025-06-25 | GSE297700 | GEO

HaCaT cells treated with bleogen pB1 or eGF

Project description:Transcriptome profiling by using RNA-seq was performed on bleogen pB1-treated, EGF-treated, and untreated HaCaT keratinocytes to gain further insights into the wound healing effects of bleogen pB1 and EGF

2022-09-15 | GSE202512 | GEO

Expression data from ependymal cell cultures treated with EGF

Project description:We identified that EGF blocks differentiation of radial glial progenitors into multiciliated cells. We evaluated global changes to ependymal cell culture gene expression profiles during EGF treatment during differentiation.

2019-05-01 | GSE124518 | GEO

EGF-induced Transcriptome Changes in GBM stem-like cells

Project description:GBM neurosphere line GBM1B were depleted of growth factors for 16 hours followed by EGF stimulation for 4 and 24 hours. RNA-seq was used to identify differentially-expressed (DE) genes after EGF treatment.

2021-04-19 | GSE151995 | GEO

Human colon cancer cell lines: NT(untreated) vs EGF, Cetuximab and Gefitinib treatments

Project description:Gene Expression Profiling of HT-29 and Caco-2 colon cancer cell lines untreated compared with EGF, Cetuximab, Gefitinib,EGF plus Cetuximab and EGF plus gefitinib treatments. Keywords: Gene Expression Profiling

2007-09-12 | GSE8967 | GEO

Astrocyte-produced HB-EGF limits autoimmune CNS pathology [WGBS]

Project description:Central nervous system (CNS) resident cells such as microglia, oligodendrocytes and astrocytes are gaining increasing attention in respect to their contribution to CNS pathologies including Multiple Sclerosis (MS). Several studies have demonstrated the involvement of pro- inflammatory glial subsets in the pathogenesis and propagation of inflammatory events in MS and its animal models. However, it has only recently become clear that the underlying heterogeneity of astrocytes and microglia can not only drive inflammation, but also lead to its resolution through direct and indirect mechanisms. Failure of these tissue-protective mechanisms may potentiate disease and increase the risk of conversion to progressive stages of MS, for which currently available therapies are limited. Using proteomic analyses of cerebrospinal fluid specimens from MS patients in combination with experimental studies, we here identify Heparin-binding EGF-like growth factor (HB-EGF) as a central mediator of tissue-protective and anti-inflammatory effects important for the recovery from acute inflammatory lesions in CNS autoimmunity. Hypoxic conditions drive the rapid upregulation of HB-EGF by astrocytes during early CNS inflammation, while pro-inflammatory conditions suppress trophic HB-EGF signaling through epigenetic modifications. Finally, we demonstrate both anti-inflammatory and tissue-protective effects of HB-EGF in a broad variety of cell types in vitro and use intranasal administration of HB-EGF in acute and post-acute stages of neuroinflammation to attenuate disease in a preclinical mouse model of MS. Altogether, we identify astrocyte-derived HB-EGF and its epigenetic regulation as a novel modulator of autoimmune CNS inflammation and potential therapeutic target in MS.

2023-12-01 | GSE245382 | GEO

C3H10T1/2 Adipogenesis: Effects of EGF and TCDD

Project description:Confluent C3H10T1/2 cells stimulated to differentiate using IDMB (1uM BRL49653, 1uM Dexamethasone, 0.5uM IBMX, 10ug/mL Insulin). Expression was examined 24 hours after IDMB treatment. Additionally, the effects of addition of TCDD 48 hours prior to IDMB treatment, and EGF addition concurrent with IDMB treatment were examined. Keywords = Adipogenesis Keywords = TCDD Keywords = EGF Keywords: repeat sample

2004-03-25 | GSE1123 | GEO

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