FOSL1- and KRAS-regulated transcriptomes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA805557 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:RNA profiling of FOSL1- and KRAS-regulated transcriptomes in human lung cancer cells harboring KRAS mutation
2023-08-10 | GSE196596 | GEO
Project description:Mutant KRAS lung adenocarcinoma cells, H2009, were depleted of FOSL1 by a specific shRNA and its transcriptome was profiled
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Project description:Despite recent advances in genomic profiling techniques, the precise mechanisms controlling GBM subtypes and their plasticity are not fully unraveled. Here,using transcriptomic data of patient derived stem cell lines we found that FOSL1 is a master regulator of the MES subtype. Depletion of FOSL1 resulted in loss of themesenchymal gene signature (MGS) in mouse Kras-mutant neural stem cells and in human brain tumor stem cells.
2020-09-30 | GSE138010 | GEO
Project description:To explore genome-wide alteration MED1 and FOSL1 after depletion of FOSL1, we performed chromatin immunoprecipitation sequencing (ChIP-seq) of SCC1 cells to examine genome-wide recruitment of MED1 and FOSL1 following FOSL1 knockdown. Depletion of FOSL1 led to dramatically loss of the recruitment of MED1 and FOSL1 at a cohort of key oncogenes associate with tumorigenesis and metastasis.
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Project description:A subset of human pancreatic ductal adenocarcinoma cells (PDACs) is characterized by high Fosl1 expression and Fosl1 is linked to the control of pro-inflammatory pathways and growth of PDAC cells. To mimick the human disease in mice (> 90% of PDAC patients harbour Kras mutations) the mutated LSL-KrasG12D allele was combined with the pancreas specific Cre recombinase Ptf1aCre (p48Cre). The two pancreatic cancer cell lines (Ptf1aCre, LSL-KrasG12D/+) were isolated from these mice and used for transcriptomics studies. The two different murine pancreatic cancer cell lines (Ptf1aCre, LSL-KrasG12D) were treated with two different Fosl1 siRNAs and one control siRNA, each. 72h after transfection a sufficient knockdown was tested by immunoblotting and qPCR. Total mRNA was isolated and checked for integrity. According to manufacture's recommendation the samples were subjected to microarray analysis using the Affymetrix Mouse Gene ST 1.0 array chip to discover differentially expressed genes.
2016-12-23 | E-MTAB-4299 | biostudies-arrayexpress
Project description:RNA-Seq of KRAS-regulated genes
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Project description:We perfromed Mint-ChIP using anti-FOSL1 antibody on Kras mutant mouse lung epithelial cells.
2021-12-22 | GSE192406 | GEO
Project description:Oncogenic KRAS drives cancer growth by activating diverse signaling networks, not all of which have been fully delineated. We set out to establish a system-wide profile of the KRAS-regulated kinase signaling network (kinome) in KRAS-mutant pancreatic ductal adenocarcinoma (PDAC). We knocked down KRAS expression in a panel of six cell lines, and then applied Multiplexed Inhibitor Bead/Mass Spectrometry (MIB/MS) chemical proteomics to monitor changes in kinase activity and/or expression. We hypothesized that depletion of KRAS would result in downregulation of kinases required for KRAS-mediated transforming activities, and in upregulation of other kinases that could potentially compensate for the deleterious consequences of the loss of KRAS. We identified 15 upregulated and 13 downregulated kinases in common across the panel. In agreement with our hypothesis, all 15 of the upregulated kinases have established roles as cancer drivers (e.g., SRC, TGFBR1, ILK), and pharmacologic inhibition of the upregulated kinase, DDR1, suppressed PDAC growth. Interestingly, 11 of the 13 downregulated kinases have established driver roles in cell cycle progression, particularly in mitosis (e.g., WEE1, Aurora A, PLK1). Consistent with a crucial role for the downregulated kinases in promoting KRAS-driven proliferation, we found that pharmacologic inhibition of WEE1 also suppressed PDAC growth. The unexpected paradoxical activation of ERK upon WEE1 inhibition led us to inhibit both WEE1 and ERK concurrently, which caused further potent growth suppression and enhanced apoptotic death than WEE1 inhibition alone. We conclude that system-wide delineation of the KRAS-regulated kinome can identify potential therapeutic targets for KRAS-mutant pancreatic cancer.
2022-02-17 | PXD025819 | Pride
Project description:The differentiation of Th17 cells is controlled by a complex network of transcription factors (TFs), including FOS and JUN proteins of the AP-1 family. The FOS-like proteins, FOSL1 and FOSL2 have recently been reported to control Th17 responses. The molecular mechanisms dictating their roles, however, are unclear. Moreover, although the functions of AP-1 TFs are largely governed by their protein-protein interactions, these are also poorly characterized in this milieu. Using affinity purification in combination with mass-spectrometry we established the first interactomes of FOSL1 and FOSL2 in human Th17 cells. In addition to their known interactions with JUN proteins, our analysis identified several novel binding partners of FOSL factors. Gene ontology analysis revealed RNA binding was enriched as the major functionality for FOSL1 and FOSL2 associated proteins, thereby suggesting possible mechanistic links that have not been studied before. Intriguingly, 29 interactors were found to be shared between FOSL1 and FOSL2, which included crucial regulators of Th17-fate. These findings, including unique and shared interactions, were validated using parallel reaction monitoring targeted mass-spectrometry (PRM-MS), with additional measurements with other laboratory methods. Overall, this study provides key insights into interaction-based signalling mechanisms of FOSL1 and FOSL2, which potentially control Th17 cell-development and associated pathologies.
2021-11-02 | PXD025729 | Pride
Project description:Primary pneumocytes from KRas;Atg5fl/+ and KRas;Atg5fl/fl littermates were cultured for 48 hours and infected with AdCre-GFP to induce expression of the KrasG12D oncogene and concomitant Atg5 deletion. The transcriptional profile of those cells was determined by mRNA sequencing and uncovered differential expression in cellular movement, inflammatory response and oxidative stress response. Comparison of transcriptomes from KRas;Atg5fl/+ and KRas;Atg5fl/fl pneumocytes
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