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Myeloid cell RelA/p65 promotes lung cancer proliferation

ABSTRACT: Smoking is the most important risk factor for both lung cancer (LC) and chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the role of myeloid cell NF-kB in the regulation of tumor cell growth signaling. We subjected mice lacking myeloid RelA/p65 to a metastatic LC model. Cigarette smoke (CS) exposure significantly increased the proliferation of Lewis lung carcinoma cell (LLC) tumors in wild type mice. In CS exposed mice lacking myeloid RelA/p65, the tumor growth was largely inhibited. Transcriptome and pathway analysis of cancer tissue revealed a fundamental impact of myeloid cells on various growth signaling pathways. Myeloid RelA/p65 is necessary to link smoke-induced inflammation with LC growth. Keywords: Expression profiling by array

ORGANISM(S): Mus musculus

PROVIDER: GSE36568 | GEO | 2012/04/01

SECONDARY ACCESSION(S): PRJNA153725

REPOSITORIES: GEO

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Myeloid cell RelA/p65 promotes lung cancer proliferation

Project description:Smoking is the most important risk factor for both lung cancer (LC) and chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the role of myeloid cell NF-kB in the regulation of tumor cell growth signaling. We subjected mice lacking myeloid RelA/p65 to a metastatic LC model. Cigarette smoke (CS) exposure significantly increased the proliferation of Lewis lung carcinoma cell (LLC) tumors in wild type mice. In CS exposed mice lacking myeloid RelA/p65, the tumor growth was largely inhibited. Transcriptome and pathway analysis of cancer tissue revealed a fundamental impact of myeloid cells on various growth signaling pathways. Myeloid RelA/p65 is necessary to link smoke-induced inflammation with LC growth. Keywords: Expression profiling by array Analysis of gene expression in lewis lung carcinoma cells resected from lungs of WT and RelA/p65 deficient mice exposed to smoke or air. Four different samples were analyzed (3 replicates each).

2012-03-31 | E-GEOD-36568 | biostudies-arrayexpress

Mouse livers lacking NF-kappaB RelA (p65) during bacteremia

Project description:Mouse livers lacking NF-kappaB RelA (p65) during bacteremia

| PRJNA522786 | ENA

Mouse livers lacking NF-kappaB RelA (p65) during bacteremia

Project description:Using a mouse model with hepatocyte-specific deletion of transcription factor NF-κB RelA (p65), our group has previously revealed the important role of RelA in inducing the acute phase response, maintaining host defense, and preventing liver injury during sepsis. To goal of this study was determine the influence of RelA on hepatic gene changes that provide liver protection during infection. Mice were generated with functional deletion of NF-kappaB RelA (p56) in hepatocytes using a Cre-LoxP system. Mutant mice expressed Cre-recombinase under the transcriptional control of an albumin promotor and homozygous floxed RelA alleles. Wild type control mice lack the Cre-recombinase. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal bacteremia.

2019-06-07 | GSE126642 | GEO

Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia

Project description:A common response to physiological duress is the hepatic acute phase response, a process during which the expression of many genes is altered in the liver. Amongst these transcripts are those encoding acute phase proteins, defined as circulating proteins with significantly changed concentrations during an acute phase response. The goal of this study was to determine the influence of NF-kappaB RelA (p65) on hepatic gene changes including but not limited to acute phase proteins during bacterial pneumonia. Using the Cre-LoxP system, mice were generated with functional deletion of NF-kappaB RelA (p65) in hepatocytes. In mutant mice, Cre-recombinase was expressed under transcriptional control of an albumin promoter in the presence of homozygous floxed alleles for RelA. Wild-type control mice lacked the Cre-recombinase transgene. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia. RNA from 2 separate groups of mice (3 mice per group) was analyzed: 1) Control mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3); and 2) Mutant mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3).

2012-02-16 | E-GEOD-35513 | biostudies-arrayexpress

Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia

2012-02-16 | GSE35513 | GEO

Trancriptome profiling of murine overexpression of p65/RelA mutants

Project description:Effect of overexpression of murine p65/RelA and D361 mutant and resulting fragments in DA1-3B Bcr-Abl+ murine cell lines

2022-07-27 | GSE98437 | GEO

p65

Project description:p65

| PRJNA811604 | ENA

Transcriptome profiling of murine overexpression of p65/RelA mutants II

Project description:Effect of overexpression of murine p65/RelA and D361 mutant and resulting fragments in B16 Bcr-Abl+ murine cell lines

2022-07-27 | GSE135136 | GEO

Transcriptome profiling of murine overexpression of p65/RelA mutants III

Project description:Effect of overexpression of murine p65/RelA and D361 mutant and resulting fragments in DA1-3B Bcr-Abl+ murine cell lines

2022-07-27 | GSE135137 | GEO

Deletion of the NF-κB subunit p65/RelA in the hematopoietic compartment leads to defects in hematopoietic stem cell function.

Project description:Deletion of the NF-κB subunit p65/RelA in the hematopoietic compartment results in gene expression changes in lineage-Flk2-c-kit+Sca-1+ cells from mouse bone marrow. We analyzed lineage-Flk2-c-kit+Sca-1+ cells from the bone marrow of p65 wild-type or knockout mice using the Affymetrix Mouse Exon 1.0 ST platform. Array data was processed by Affymetrix Exon Array Computational Tool. No technical replicates were performed.

2013-04-04 | E-GEOD-45755 | biostudies-arrayexpress

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