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RNA-Seq analysis of the impact of a kinase NIK inhibitor (DMBP5) on the human melanoma cell line A375

ABSTRACT: Introduction: there is growing evidence that the IFN- -related cytokine signature plays a major role supporting the effect of pharmacological blockade of immune checkpoints. The expression of IFN- in cancer cells is repressed by several factors, among them a key role is played by the oncogene EZH2, which in turns is controlled by the non-canonical NF-kB pathway and its upstream kinase, NIK. Methodology: we developed a series of NIK inhibitors and compared the effects on cancer cells of one of them (DMBP5) to an siRNA against NIK via transcriptomic analysis (RNA-seq). Results: mRNA modifications induced by DMBP5 on A375 melanoma cells closely resemble the ones observed with siRNA against NIK. Conclusions: DMBP5 is a very selective and effective non-competitive NIK inhibitor (first in class).

ORGANISM(S): Homo sapiens

PROVIDER: GSE106286 | GEO | 2020/01/08

REPOSITORIES: GEO

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RNA-Seq analysis of the impact of a kinase NIK inhibitor (DMBP5) on the human melanoma cell line A375 (replicate 2).

Project description:Introduction: there is growing evidence that the IFN-γ-related cytokine signature plays a major role supporting the effect of pharmacological blockade of immune checkpoints. The expression of IFN-γ in cancer cells is repressed by several factors, among them a key role is played by the oncogene EZH2, which in turns is controlled by the non-canonical NF-kB pathway and its upstream kinase, NIK. Methodology: we developed a series of NIK inhibitors and compared the effects on cancer cells of one of them (DMBP5) to an siRNA against NIK via transcriptomic analysis (RNA-seq). Results: mRNA modifications induced by DMBP5 on A375 melanoma cells closely resemble the ones observed with siRNA against NIK. Conclusions: DMBP5 is a very selective and effective non-competitive NIK inhibitor (first in class).

2020-01-08 | GSE106285 | GEO

RNA-Seq analysis of the impact of a kinase NIK inhibitor (DMBP5) on the human melanoma cell line A375 (replicate 1)

2020-01-08 | GSE101637 | GEO

NIK expression stimulated G6PD phosphorylation

Project description:Our findings establish NIK as a pivotal regulator of T cell metabolism in anti-tumor immunity and highlight a posttranslational mechanism of metabolic regulation involving the G6PD-NADPH redox system. CoIP assays revealed a strong physical interaction between NIK and G6PD in both T cells and transiently transfected 293 cells, suggesting G6PD to be a direct target of NIK. Using a phosphoprotein gel analysis approach, we demonstrated that NIK expression stimulated G6PD phosphorylation. To further study the mechanism, we performed mass spectrometry identify phosphorylation sites of G6PD stimulated by NIK

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Gene expression profile in A375 melanoma cells after 45 functionally important molecules were knocked down using siRNA

Project description:Affymetrix microarray data were generated from A375 melanoma cells treated in vitro with siRNAs against 45 transcription factors and signalling molecules. 45 functionally important molecules were knocked down in A375 melanoma cells by siRNA. Then the gene expression profiles of these A375 cells, along with untreated cells and sRNA control treated cells were analysed by microarrays.

2012-03-15 | E-GEOD-31534 | biostudies-arrayexpress

The NFKB inducing kinase (NIK) modulates hematopoiesis during stress

Project description:The genetic programs that maintain hematopoiesis during steady state in physiologic conditions are different from those activated during stress. Here we show that hematopoietic stem cells (HSCs) with deficiencies in components of the alternative NFkB pathway (the NFkB inducing kinase, NIK, and the downstream molecule NFkB2) had a defect in response to stressors such as supraphysiological doses of cytokines, chemotherapy and hematopoietic transplantation. NIK-deficient mice had peripheral blood and bone marrow leukocyte numbers within normal ranges (except for the already reported defects in B-cell maturation), however, HSCs showed significantly slower expansion capacity in in vitro cultures compared to wild type HSCs. This was due to a delayed cell cycle and increased apoptosis. In vivo experiments showed that NIK-deficient HSCs did not recover at the same pace as controls when challenged with myeloablative chemotherapy. Finally, NIK-deficient HSCs showed a significantly decreased competitive repopulation capacity in vivo. Using HSCs from mice deficient in one of two downstream targets of NIK, i.e., either NFkB2 or c-Rel, only NFkB2 deficiency recapitulated the defects detected with NIK-deficient HSCs. Our results underscore the role of NIK and the alternative NFkB pathway for the recovery of normal levels of hematopoiesis after stress.

2014-11-29 | GSE63702 | GEO

NFATC2 knock-down on melanoma cell line A375

Project description:RNA-seq on NFATC2 knock-down (siRNA) on melanoma cell line A375

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Gene expression changes in A375 melanoma cells in response to ERK3 knockdown.

Project description:Gene expression microarrays were used to compare A375 cells treated with a control siRNA or an siRNA targeting ERK3 (MAPK6).

2019-03-01 | GSE112040 | GEO

Constitutive activation of the receptor-like kinase NIK impairs translation and confers tolerance to begomovirus infection

Project description:To generate an efficient defense against begomovirus, we modulated the activity of the immune defense receptor NIK (NSP-Interacting Kinase) in tomato plants; NIK is a virulence target of the begomovirus NSP during infection. Replacing threonine-474 with aspartate (T474D) within the kinase activation loop promoted the constitutive activation of NIK-mediated defenses. This activation resulted in the down-regulation of translation-related genes and the suppression of global translation in T474D-overexpressing tomato lines. We also found that T474D-induced defense-related transcripts were associated with polysomes and immune proteins, which accumulated to detectable levels in T474D leaves. Consistent with these findings, T474D transgenic lines were tolerant to the tomato-infecting begomoviruses ToYSV and ToSRV. We propose that NIK mediates an anti-viral response via translation suppression and immune system induction. Global variation on gene expression induced by NIK expression and virus infection using total RNA from mock-inoculated and ToYSV-infected tomato wild-type plants, mock-inoculated and infected 35S::NIK1-4 overexpressing lines and mock-inoculated and infected 35S::T474D overexpressing lines. File map_itag23.csv correlates the ITAG 2.3 cDNA ID with the 21 bp reads in file Profiles_with_differential_expressions.csv.

2013-12-17 | E-GEOD-38028 | biostudies-arrayexpress

Comparasion between MCF7-NIK overexpressing cells, MCF7-control cells and MCF7-NIK depleted cells

Project description:Analysis of differentially expressed genes in MCF7 cancer cells transfected with an expression vector containing the ORF of NIK, a shRNA of NIK and a control shRNA. Transient transfections were performed in triplicates . We use micorarrays to elucidate the machanisms by which NIK regulates stem cells biology

2015-11-30 | GSE63382 | GEO

RNA-seq Analysis of Transcriptomes in β-Gal-overexpressing, NIK-overexpressing, and NIK(KA)-overexpressing αTC1-6 cells

Project description:Purpose: The goal of this study is to determine the molecular mechanisms involved in the NIK regulation of α cell function. Methods: mRNA profiles of β-Gal control, NIK, and NIK(KA) overexpressed αTC1-6 cells were generated by deep sequencing using an Illumina Hiseq platform. Paired-end clean reads were aligned to the mouse reference genome(Ensemble_GRCm38.89) with TopHat (version 2.0.12), and the aligned reads were used to quantify mRNA expression by using HTSeq-count (version 0.6.1). Conclusion: Our study represents the first detailed analysis of NIK-overexpressing aTC1-6 cell transcriptomes, generated by RNA-seq technology. Our results show that 328 genes were upregulated and 48 genes were downregulated following NIK overexpression. GO analysis indicated that the upregulated genes were primarily related to the immune response. KEGG pathway enrichment analysis showed that immune signaling pathways, including the TNF, NF-κB, and chemokine signaling pathways, were significantly activated by NIK overexpression in aTC1-6 cells, while genes related to metabolism-associated signal pathways were significantly decreased. NIK(KA), the dominant-negative mutant of NIK, does not affect gene expression in aTC1-6 cells.

2018-12-30 | GSE112511 | GEO

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