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Expression data from cultured mouse BALB 3T3 cells containing bacterial plasmid gene mucAB

ABSTRACT: The gene mucAB has an error-prone activity in bacteria. We introduced mucAB into mouse 3T3 cells with an expression vector and found drastic increase of spontaneous transformation, accompanied by increase of expression of eight oncogenes, i. e., Gpnmb, Foxml, Maff, Myc, Aurka, Aukb, Fosl1, and Anxa8 and decrease of expression in two oncogenes, i. e., Lrig1 and RhoX in order of the magnitude of change, as compared with those in non-treated 3T3 cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE42927 | GEO | 2013/12/01

SECONDARY ACCESSION(S): PRJNA183882

REPOSITORIES: GEO

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Expression data from cultured mouse BALB 3T3 cells containing bacterial plasmid gene mucAB

Project description:The gene mucAB has an error-prone activity in bacteria. We introduced mucAB into mouse 3T3 cells with an expression vector and found drastic increase of spontaneous transformation, accompanied by increase of expression of eight oncogenes, i. e., Gpnmb, Foxml, Maff, Myc, Aurka, Aukb, Fosl1, and Anxa8 and decrease of expression in two oncogenes, i. e., Lrig1 and RhoX in order of the magnitude of change, as compared with those in non-treated 3T3 cells. Transformation of cultured mouse BALB 3T3 cells was used as an indicator of cellular oncogenesis. We examined effects of introduction of foreign bacterial plasmid gene into mouse cells on spontaneous transformation frequency, accompanied by change of expression of known oncogenes. To do this, 3T3 cells with or without mucAB were compared for expression of known genes, using the microarray method.

2013-12-01 | E-GEOD-42927 | biostudies-arrayexpress

ChIP-seq analysis of MED1 and FOSL1 in SCC1 cells after depletion of FOSL1

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.

2021-04-14 | GSE151132 | GEO

LRIG1 engages ligand VISTA and impairs tumor-specific CD8+ T cell responses

Project description:Cancer immunotherapies boost antitumor immunity and improve the survival of cancer patients. V-domain Immunoglobulin Suppressor of T cell Activation (VISTA) is an immune 20 checkpoint target but presents elusive signaling mechanisms. We report a novel VISTA binding partner, Leucine-Rich Repeats and Immunoglobulin Like Domains 1 (LRIG1), which acts as an inhibitory receptor by engaging VISTA and suppressing T cell receptor signaling pathways. Mice with T cell-specific LRIG1 deletion developed superior antitumor T cell responses. Mechanistically, LRIG1-deficient tumor-specific CD8+ cytotoxic T cells (CTLs) exhibited longer 25 persistence due to improved expansion and survival and greater effector function. Sustained tumor control was also associated with a reduction of quiescent CTLs (TCF1+ CD62Lhi PD-1low) and a reciprocal increase in progenitor and memory-like CTLs (TCF1+ PD-1+). In human melanoma, an elevated LRIG1 expression on tumor-infiltrating CD8+ CTLs correlated with resistance to immunotherapies. Taken together, these results delineate the role of LRIG1 as an inhibitory 30 immune checkpoint receptor and propose a rationale for targeting the VISTA/LRIG1 axis for cancer immunotherapy.

2024-10-17 | PXD050084 | Pride

Expression microarray analysis of RHOXF1 and RHOXF2 transfected HEK293 cells

2016-07-16 | GSE84463 | GEO

Comparison of gene expression profiles of MafF-/-: MafG-/-: MafK-/- embryos and MafF-/-: MafG+/+: MafK-/- embyos

Project description:MafF-/-: MafG+/+: MafK-/- mice are viable, while MafF-/-: MafG-/-: MafK-/- mice are embryonic lethal. To get an insight into the cause of the lethality of small Maf triple knockout mice, transcriptome analysis was performed using whole embyos of MafF-/-: MafG-/-: MafK-/- at E10.5 and those of MafF-/-: MafG+/+: MafK-/- at E9.5 or E10.5. Because MafF-/-: MafG-/-: MafK-/- embryos exhibit growth retardation, the gene expression profile of MafF-/-: MafG-/-: MafK-/- embryos at E10.5 was compared with that of MafF-/-: MafG+/+: MafK-/- embyos at E9.5. The gene expression profile of MafF-/-: MafG+/+: MafK-/- embryos at E10.5 was also examined as an alternative control. Total RNA was prepared from pooled three embryos for each sample.

2012-01-09 | E-GEOD-29558 | biostudies-arrayexpress

LRIG1 is a gatekeeper to exit from quiescence in adult neural stem cells

Project description:Adult neural stem cells (NSCs) must tightly regulate quiescence and proliferation. Single cell analysis has suggested a continuum of cell states as NSCs exit quiescence. Here we capture and characterize in vitro primed quiescent NSCs and identify LRIG1 as an important regulator. We show that BMP-4 signaling induces a dormant non-cycling quiescent state (d-qNSCs), whereas combined BMP-4/FGF-2 signalling induces a distinct primed quiescent state poised for cell cycle re-entry. Primed quiescent NSCs (p-qNSCs) are defined by high levels of LRIG1 and CD9, as well as an interferon response signature, and can efficiently engraft into the adult subventricular zone (SVZ) niche. Genetic disruption of Lrig1 in vivo within the SVZ NSCs leads an enhanced proliferation. Mechanistically, LRIG1 primes quiescent NSCs for cell cycle re-entry and EGFR responsiveness by enabling EGFR protein levels to increase but limiting signaling activation. LRIG1 is therefore an important functional regulator of NSC exit from quiescence.

2021-03-18 | GSE168189 | GEO

Expression microarray analysis of RHOXF1 and RHOXF2 transfected HEK293 cells

Project description:The X-linked reproductive homeobox (RHOX) gene cluster encodes transcription factors displaying preferential expression in reproductive tissues. They have important roles in human male fertility based on phenotypic defects of Rhox-mutant mice and the finding that aberrant RHOX promoter methylation is strongly associated with abnormal human sperm parameters. The aim of this study was to analyze the molecular mechanism of RHOX action in humans. Using genome-wide analysis, we investigated the identity of genes regulated by the known human RHOX transcription factors: RHOXF1 and RHOXF2/2B. HEK293 cells were transiently transfected with either RHOX expression (RHOXF1; RHOXF2) or an empty control vector. Afterwards, differently expressed genes were identified by microarray analysis after 24h and 48h of transfection. Thereby we could identify genes that are differently regulated in response to RHOX overexpression. Total RNA was isolated from RHOX (RHOXF1; RHOXF2) and control transfected HEK293 cells after 24h and 48h of transfection. Affymetrix GeneChip Human Exon 1.0 ST arrays were used to evaluate changes in mRNA expression in RHOX transfected samples compared to control transfected samples (analyzed in biological triplicates). Data were processed and analyzed using Affymetrix Gene Expression Console and Affymetrix transcriptome analysis console.

2016-07-16 | E-GEOD-84463 | biostudies-arrayexpress

Aurora A kinase Inhibition Reprograms Metabolism dependent on PGC1α to Drive Synthetic Lethality with Fatty Acid Oxidation Inhibition in Glioblastoma [ChIP-Seq]

Project description:By integration of transcriptome, CHIP-seq, ATAC-seq, proteomic and metabolite screening followed by carbon tracing (U-13C-Glucose, U-13C-Glutamine and U-13C-Palmitic acid) and extracellular flux analysis we provided evidence that genetic (shRNA and CRISPR/Cas9) and pharmacological (Alisertib) AURKA inhibition elicited substantial metabolic reprogramming supported in part by inhibition of MYC targets and concomitant activation of PPARA signaling. While glycolysis was suppressed by AURKA inhibition, we noted a compensatory increase in oxygen consumption rate fueled by enhanced fatty acid oxidation (FAO). Whereas interference with AURKA elicited a suppression of c-Myc, we detected an upregulation of PGC1α, a master regulator of oxidative metabolism, upon AURKA inhibition. Chromatin immunoprecipitation experiments confirmed binding of c-Myc to the promoter region of PGC1α, which is abrogated by AURKA inhibition and in turn unleashed PGC1α expression. To interfere with this oxidative metabolic reprogramming, we combined AURKA inhibitors with inhibitors of FAO (etomoxir) and electron transport chain (gamitrinib) and found substantial synergistic growth inhibition in patient derived xenograft in vitro and extension of overall survival without induction of toxicity in normal tissue.

2021-06-01 | GSE161573 | GEO

Aurora A kinase Inhibition Reprograms Metabolism dependent on PGC1α to Drive Synthetic Lethality with Fatty Acid Oxidation Inhibition in Glioblastoma [ATAC-Seq]

2021-06-01 | GSE161572 | GEO

Expression data from mouse ES cells after control RNAi (scramble siRNAs) or RNAi specific for Kdm6a treatment.

Project description:To address the functional role of KDM6A in the regulation of Rhox genes, male and female mouse ES cells were transfected with a mixture of three small interfering RNA duplexes, each of which targets a different region of Kdm6a mRNA. We found that Kdm6a knockdown in mouse ES cells caused a decrease in expression of a subset of Rhox genes, Rhox6 and 9. Furthermore, Rhox6 and 9 expression was decreased in female ES cells but not male ES cells indicating that KDM6A regulates Rhox gene expression in a sexually dimorphic manner.

2013-03-13 | GSE45034 | GEO

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