Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA153725 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
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
2012-04-01 | GSE36568 | GEO
Project description:Trancriptome profiling of murine overexpression of p65/RelA mutants
| PRJNA385097 | ENA
Project description:Pancreatic neuroendocrine tumours (PNETs) are graded based on their proliferation rate marked by Ki-67, where increased proliferation is associated with poorer prognosis. However, detailed molecular mechanisms underlying their proliferation remain to be clarified. In this study, we have identified NF-κB signalling as a novel pathway that is hyperactivated in PNETs via single cell analyses and immunofluorescence staining of human PNET tissues. Furthermore, we have confirmed that the NF-κB subunit RelA/p65 is implicated in PNET proliferation in vitro and in vivo and demonstrated that depleting or inhibiting RelA/p65 significantly reduces the proliferation rate of QGP-1 cells. Separately, we have uncovered that menin (encoded by the MEN1 gene), a tumour suppressor commonly mutated in PNETs, represses PNET proliferation in a RelA/p65-dependent manner, by downregulating the expression of RelA/p65 target genes associated with proliferation. We have identified the NR4A1 gene as one such target and confirmed that its expression is highly upregulated in MEN1 mutated PNETs. Additionally, the depletion or chemical inhibition of NR4A1 significantly reduced cellular proliferation. Therefore, serving as a proof of concept that RelA/p65 target genes such as NR4A1 is implicated in PNET proliferation and can be targeted for therapeutic treatment. Overall, our study has identified the NF-κB signalling pathway and a subset of its genes such as NR4A1 to be responsible for PNET proliferation, opening new potential therapeutic options for both PNETs and MEN1-mutated PNETs.
2026-09-17 | GSE242549 | GEO
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2021-05-05 | PXD022309 | Pride
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2018-04-24 | PXD007288 | Pride
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Purpose: To study the alteration of whole transcriptome of Lewis lung carcinoma (LLC) cells after the decreasing of malignant properties of tumor by treatment of tumor-bearing mice with RNase A. Methods: Whole transcriptome profile of Lewis lung carcinoma before and after RNase A treatment were generated by deep sequencing using SOLiD 5.5. The sequence reads were mapped by Bioscope 1.3 software, differential expression was evaluated by Cufflinks v.2.0.1 package. Results: Difference in expression was found for 966 genes. Conclusions: Our study represents the first detailed analysis of alteration of transcriptome of Lewis lung carcinoma after the decrease of malignant prtoperties of the tumor (proliferation and invasion) by RNase A.
2014-12-03 | GSE63758 | GEO
Project description:Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia
| PRJNA156107 | ENA
Project description: Not available
| S-EPMC11335981 | biostudies-literature