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Gene expression of inflammatory monocytes/macrophages after ablative radiotherapy in pancreatic adenocarcinoma

ABSTRACT: Ablative RT results in increased expression of CCL2 within the tumor microenvironment of pancreatic ductal adenocarcinoma (PDAC) and also increased recruitment of CD45+CD11b+Ly6Chi inflammatory monocytes/macrophages. This increase in CCL2 expression and recruitment of inflammatory monocytes/macrophages is a mechanism of resistance to the anti-tumor effects of ablative radiotherapy (RT). We used microarrays to study changes in gene expression patterns of inflammatory monocytes/macrophages sorted from the tumor microenvironment after ablative RT in a subcutenous model of pancreatic adenocarcinoma. From this, we identified 8 genes with an absolute fold change of expression equal to or greater than 2 with a false discovery rate equal to or less than 25 %.

ORGANISM(S): Mus musculus

PROVIDER: GSE82276 | GEO | 2016/08/01

SECONDARY ACCESSION(S): PRJNA324536

REPOSITORIES: GEO

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Gene expression of inflammatory monocytes/macrophages after ablative radiotherapy in pancreatic adenocarcinoma

Project description:Ablative RT results in increased expression of CCL2 within the tumor microenvironment of pancreatic ductal adenocarcinoma (PDAC) and also increased recruitment of CD45+CD11b+Ly6Chi inflammatory monocytes/macrophages. This increase in CCL2 expression and recruitment of inflammatory monocytes/macrophages is a mechanism of resistance to the anti-tumor effects of ablative radiotherapy (RT). We used microarrays to study changes in gene expression patterns of inflammatory monocytes/macrophages sorted from the tumor microenvironment after ablative RT in a subcutenous model of pancreatic adenocarcinoma. From this, we identified 8 genes with an absolute fold change of expression equal to or greater than 2 with a false discovery rate equal to or less than 25 %. A pancreatic cancer tumor cell line derived from spontaneously arising tumors in KrasLSL-G12D/+, Trp53LSL-R172H/+, Pdx1-Cre (KPC) mice was subcutaneously implanted into 8 week old female C57BL/6 and allowed to grow for 14 days. After 14 days, 4 mice received 20 Gy of radiation, and 4 mice received a sham treatment. One day post treatment, tumors were harvested, and inflammatory monocytes/macrophages were isolated using flow sorting based on a surface expression phenotype of CD45+ CD11b+ Ly6Chi. From this cell population, total RNA was extracted for creation of cDNA and hybridization on Affymetrix microarrays. From the microarrays, a set of genes associated with radiation treatment of PDAC was identified.

2016-08-01 | E-GEOD-82276 | biostudies-arrayexpress

Mus musculus

Project description:Gene expression of inflammatory monocytes/macrophages after ablative radiotherapy in pancreatic adenocarcinoma

| PRJNA324536 | ENA

Gene expression in PBMCs of patients with hepatocarcinoma: effect of ablative treatment - genes

Project description:Gene expression profiles of PBMCs in patients with hepatocarcinoma after ablative treatment. Results provide the information of changes in PBMPs transcriptome following ablative treatment of hepatocarcinoma.

2020-01-04 | GSE143004 | GEO

Inhibitor of NFκB ζ (IκBζ) is a transcriptional key regulator of monocyte chemoattractant protein-1 (MCP-1/CCL2)

Project description:Monocyte chemoattractant protein 1 (MCP-1/CCL2) is critically involved in directing the migration of blood monocytes to sites of inflammation. Consequently, excessive MCP-1 secretion has been linked to many (auto)inflammatory diseases, whereas a lack of expression severely impairs immune responsiveness. We demonstrate that the atypical inhibitor of NF-κB ζ (IκBζ), a transcriptional co-activator required for the selective expression of a subset of NF-κB target genes, is a key activator of the Ccl2 gene. IκBζ-deficient macrophages exhibited impaired secretion of MCP-1 when challenged with diverse inflammatory stimuli, such as lipopolysaccharide or peptidoglycan. These findings were reflected at the level of Ccl2 gene expression, which was tightly coupled to the presence of IκBζ. Moreover, mechanistic insights acquired by chromatin immunoprecipitation demonstrate that IκBζ is directly recruited to the proximal promoter region of the Ccl2 gene and required for histone H3K9 trimethylation. Finally, IκBζ-deficient mice showed significantly impaired MCP-1 secretion and monocyte infiltration in an experimental model of peritonitis. Together, these findings suggest a distinguished role of IκBζ in mediating the targeted recruitment of monocytes in response to local inflammatory events. Peritoneal macrophages from Wildtype and IκBζ-Knockout mice were either stimulated with 1µg/ml LPS for 4h or left untreated (triplicates each)

2013-04-09 | E-GEOD-43075 | biostudies-arrayexpress

Deciphering the molecular effects of non-ablative Er:YAG laser treatment in an in vitro model of the non-keratinized mucous membrane

Project description:This study aimed to investigate the molecular effects of non-ablative Er:YAG laser treatment using an in vitro model of the non-keratinized mucous membrane and to compare its molecular effects with other ablative and non-ablative laser systems. In dermatology, the use of non-ablative and ablative fractional lasers has become the gold standard treatment for a number of indications. Each of the individual laser types is advantageous for different types of indications due to its respective properties, but new technologies open up new fields of application for individual laser systems. Performing a comprehensive gene expression profiling we compared the gene regulatory effects of non-ablative Er:YAG laser with other non-ablative and ablative laser systems. In vitro 3D models have proven to be a reliable and reproducible tool to study the molecular biological effects of different laser settings.

2020-06-01 | GSE151041 | GEO

Exploratory Study to Identify Skin Anti-Aging Biomarkers as a Result of a Non-ablative Fractional Laser Treatment

Project description:Non-ablative fractional laser can be used to treat photoaged skin by stimulating the breakdown and regeneration of dermal matrix constituents, such as collagen and elastic fibers. The objective of this study was to validate previously studied molecular mechanisms and explore yet uncharacterized biomarkers underlying the clinical efficacy of non-ablative fractional laser resurfacing.

2022-12-09 | GSE206495 | GEO

Tumor-associated macrophages regulate the gene expression profiles of pancreatic cancer cells both under normoxia and hypoxia

Project description:Pancreatic cancer is a devastating and intractable disease with highly lethal rate, which is equal to incidence of the disease.It is well established that tumor microenvironment plays a pivotal role in tumor progression and metastasis.Tumor-associated macrophages (TAMs) are frequently found in close proximity with pancreatic cancer cells, but it is uncertain whether they are involved in pancreatic cancer progression.TAMs around the cancer regions usually exert their tumor-supporting functions by the secretion of cytokines and inflammatory mediators.In this study, we aim to investigate that whether tumor-associated macrophages regulate the gene expression profiles of pancreatic cancer cells both under normoxia and hypoxia.

2018-05-07 | GSE109110 | GEO

Inhibitor of NFκB ζ (IκBζ) is a transcriptional key regulator of monocyte chemoattractant protein-1 (MCP-1/CCL2)

2013-04-09 | GSE43075 | GEO

Noncanonical pathway for regulation of CCL2 expression by an mTORC1-FOXK1 axis promotes recruitment of tumor-associated macrophages

Project description:C-C chemokine ligand 2 (CCL2) plays pivotal roles in tumor formation, progression, and metastasis. Although CCL2 expression has been found to be dependent on the nuclear factor (NF)–κB signaling pathway, the regulation of CCL2 production in tumor cells has remained unclear. Mammalian target of rapamycin complex 1 (mTORC1) is a protein kinase that is activated in various tumor cell types. We have now identified a noncanonical pathway for regulation of CCL2 production that is mediated by mTORC1 but independent of NF-κB. Multiple phosphoproteomics approaches identified the transcription factor forkhead box K1 (FOXK1) as a downstream target of mTORC1, with dephosphorylation of FOXK1 in response to mTORC1 activation resulting in transactivation of the CCL2 gene. Inhibition of the mTORC1-FOXK1 axis attenuated insulin-induced CCL2 production as well as the accumulation of tumor-associated monocytes-macrophages and tumor progression in mice. Our results suggest that FOXK1 directly links mTORC1 signaling and CCL2 expression in a manner independent of NF-κB, and that CCL2 produced by this pathway contributes to tumor progression. Specific inhibition of FOXK1 may thus be a potential therapeutic strategy for cancer.

2017-11-30 | PXD007996 | Pride

Macrophage development and activation involve coordinated intron retention in key inflammatory regulators

Project description:Monocytes and macrophages are essential components of the innate immune system. Herein, we report that intron retention (IR) plays an important role in the development and function of these cells. Using mRNA sequencing, bioinformatics analyses and RT-qPCR validation, we identified differential IR and altered expression of key genes involved in macrophage development and function, both in vitro and in vivo. We demonstrate that decreased IR in nuclear-detained mRNA is coupled to increased expression of genes encoding regulators of macrophage transcription, phagocytosis and inflammatory signalling, including ID2, IRF7, ENG and LAT. We further show that this dynamic IR program persists during the polarisation of resting macrophages into activated macrophages. In the presence of proinflammatory stimuli, intron-retaining CXCL2 and NFKBIZ transcripts in macrophages are rapidly spliced, leading to timely expression of these key inflammatory regulators by macrophages. Our study provides novel insights into the molecular mechanisms controlling vital regulators of the innate immune response.

2020-05-27 | PXD017391 | Pride

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