NF-kB associated markers of PD-1 immunotherapy response in early and metastatic triple negative breast cancer
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE279896 | GEO | 2024/10/30
REPOSITORIES: GEO
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Project description:Analysis of human triple-negative breast cancer cells (TNBCs) which have high NF-kB activity. Proteins derived from NF-κB target genes might be molecular targets for cancer therapy. Results provide new insights into tumor proliferation mechanisms.
2015-02-20 | GSE56812 | GEO
Project description:Analysis of human triple-negative breast cancer cells (TNBCs) which have high NF-kB activity. Proteins derived from NF-κB target genes might be molecular targets for cancer therapy. Results provide new insights into tumor proliferation mechanisms. Exp. 1: Mock MDA-MB-436 cells vs. MDA-MB-436 cells infected with Adenovirus-IkBaSR; Exp. 2: MDA-MB-436 cells infected with Adenovirus-GFP vs. MDA-MB-436 cells infected with Adenovirus-IkBaSR.
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Project description:2 This project is to identify the potential neddylation sites in human NF-kB inducing kinase (A.k.a. Map3K14). NIK-HA or NIK-HA in combination with FLAG-NEDD8 were co-expressed in HEK293T cells. NIK-HA were pulled down via denaturing immunoprecipitation protocol, subject to SDS-PAGE, in-gel trypsin digestion, and Nano LC-MS/MS Analysis. The potential peptides containing K-GG sites were identified.
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Project description:This study identifies mechanisms of response to immune checkpoint inhibition in mouse models of triple negative breast cancer.
2019-11-13 | GSE136206 | GEO
Project description:EZH2 has been studied most extensively in the context of PRC2-dependent gene repression. Paradoxically, accumulating evidence indicates non-canonical functions for EZH2 in cancer contexts including promoting gene expression in triple negative breast cancer (TNBC) cells through interactions with the transcription factor NF-kB. We define a genomic profile of EZH2 and NF-kB factor RelA, RelB, and NFKB2/p52 co-localization and positive regulation of a subset of NF-kB targets and genes associated with oncogenic functions in TNBC, which is enriched in patient datasets. We demonstrate interaction between EZH2 and RelA requiring the recently identified EZH2 transactivation domain (TAD), which mediates EZH2 recruitment to and activation of certain NF-kB-dependent genes, and supports downstream stemness phenotypes in TNBC cells. Interestingly, EZH2-NF-kB positive regulation of genes and stemness does not require PRC2. This study provides new insight into pro-oncogenic regulatory functions for EZH2 in breast cancer through PRC2-independent, and NF-kB-dependent regulatory mechanisms.
2023-07-10 | GSE223959 | GEO
Project description:Analysis of human triple-negative breast cancer cells (TNBCs) which have high NF-kB activity. Proteins derived from NF-κB target genes might be molecular targets for cancer therapy. Results provide new insights into tumor proliferation mechanisms. Exp. 1: Mock MDA-MB-436 cells vs. MDA-MB-436 cells infected with Adenovirus-IkBaSR; Exp. 2: MDA-MB-436 cells infected with Adenovirus-GFP vs. MDA-MB-436 cells infected with Adenovirus-IkBaSR.
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Project description:To address the role of NF-kB in aging in vivo, we utilized a well-characterized system that allows inducible and site-specific inhibition of NF-kB activity in murine skin. The hormone binding domain of the mutant estrogen receptor that is responsive to 4-hydroxytamoxifen (4-OHT) was fused to a mutant of p50 (IDNkB, inducible dominant negative NF-kB) that dimerizes with other NF-kB subunits but is unable to bind DNA, thus dominantly inhibiting NF-kB activity. Expression was driven within the basal layer of murine epidermis by the keratin 14 promoter in transgenic mice. To test whether NF-kB activity is required to maintain age-associated gene expression, we applied topical 4-OHT and ethanol vehicle (EtOH) for two weeks to the right (R) and left (L) dorsal flanks, respectively, of chronologically aged transgenic mice (O, 18-23 months). Young transgenic mice (Y, 1 month) were treated in parallel as control. Skin samples were harvested and analyzed for gene expression using mouse cDNA microarrays containing 35,217 elements, representing 18,880 unique genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set Computed
2010-06-30 | E-GEOD-3845 | biostudies-arrayexpress
Project description:To address the role of NF-kB in aging in vivo, we utilized a well-characterized system that allows inducible and site-specific inhibition of NF-kB activity in murine skin. The hormone binding domain of the mutant estrogen receptor that is responsive to 4-hydroxytamoxifen (4-OHT) was fused to a mutant of p50 (IDNkB, inducible dominant negative NF-kB) that dimerizes with other NF-kB subunits but is unable to bind DNA, thus dominantly inhibiting NF-kB activity. Expression was driven within the basal layer of murine epidermis by the keratin 14 promoter in transgenic mice. To test whether NF-kB activity is required to maintain age-associated gene expression, we applied topical 4-OHT and ethanol vehicle (EtOH) for two weeks to the right (R) and left (L) dorsal flanks, respectively, of chronologically aged transgenic mice (O, 18-23 months). Young transgenic mice (Y, 1 month) were treated in parallel as control. Skin samples were harvested and analyzed for gene expression using mouse cDNA microarrays containing 35,217 elements, representing 18,880 unique genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
2007-12-01 | GSE3845 | GEO
Project description:The nuclear factor kB (NF-kB) subunits RelA, RelB, c-Rel, p50 and p52 are each critical for B-cell development and function. To systematically characterize their responses to canonical and non-canonical NF-kB pathways activity, we performed ChIP-seq analysis in lymphoblastoid B-cells. We found a surprisingly complex NF-kB binding landscape, which did not readily reflect the two NF-kB pathway paradigm. Instead, ten subunit binding patterns were observed at promoters and eleven at enhancers. Surprisingly, nearly one-third of NF-kB binding sites lacked kB motifs. De novo motif finding uncovered distinct modes of NF-kB recruitment at these sites. The oncogenic forkhead box protein FOXM1 and NF-kB co-occupied many kB sites despite the absence of a FOXM1 DNA motif. FoxM1 knockdown decreased expression of key NF-kB targets and caused apoptosis. Our study highlights opportunities for selective therapeutic NF-kB blockade.
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