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Homo sapiens

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

PROVIDER: PRJNA395046 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5839971_1.fastq.gz	Fastqsanger.gz
	SRR5839971_2.fastq.gz	Fastqsanger.gz
	SRR5839972_1.fastq.gz	Fastqsanger.gz
	SRR5839972_2.fastq.gz	Fastqsanger.gz
	SRR5839973_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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

| PRJNA416128 | ENA

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

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

| PRJNA416122 | ENA

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

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 | GSE101637 | GEO

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

Project description: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).

2020-01-08 | GSE106286 | GEO

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

2020-01-08 | GSE106285 | GEO

Impact of BRAF kinase inhibitors on miRNomes and transcriptomes of melanoma cells (gene expression dataset)

Project description:Melanoma is an aggressive skin cancer with increasing incidence worldwide. The development of BRAF kinase inhibitors as targeted treatments for patients with BRAF-mutant tumours contributed profoundly to an improved overall survival of patients with metastatic melanoma. Despite these promising results, the emergence of rapid resistance to targeted therapy remains a serious clinical issue. To investigate the impact of BRAF inhibitors on miRNomes and transcriptomes, we used in vitro melanoma models consisting of BRAF inhibitor-sensitive and -resistant cell lines generated in our laboratory. miRNA and gene expression were assessed by microarray analyses of the BRAF inhibitor sensitive melanoma cells A375, IGR37, and 501Mel, as well as on the vemurafenib (PLX4032) - resistant cells A375_XP, IGR37_XP, 501Mel_XP, and dabrafenib (GSK2118436) - resistant cells A375_GP, IGR37_GP, 501Mel_GP. For each cell line the microarray experiment was performed in duplicates.

2017-03-06 | E-MTAB-5511 | biostudies-arrayexpress

Impact of BRAF kinase inhibitors on miRNomes and transcriptomes of melanoma cells (miRNA dataset)

2017-03-06 | E-MTAB-5510 | biostudies-arrayexpress

Gene expression of the A375 melanoma cell line treated with RAF inhibitors Vemurafenib and time-course with EGF stimulation during Vemurafenib RAF inhibitor treatment alone or with the MEK inhibitor Cobimetinib

Project description:We treated for 24 hours the BRAF-V600E melanoma cell line A375 with 7 doses of the RAF inhibitor Vemurafenib and, in a second experimental desing, we treated for 24 hours the BRAF-V600E melanoma cell line A375 with Vemurafenib (1 uM) alone or in combination with the MEK inhibitor Cobimetinib (1 uM) and subsequently stimulated with EGF in a time-course of 7 time points for up to 8 hours (0, 0.5, 1, 2, 3, 4, 8 hours).

2020-10-19 | GSE127988 | GEO

Neratinib, a Pan ERBB/HER Inhibitor, Restores Sensitivity of PTEN-null, BRAFV600E Melanoma to BRAF/MEK Inhibition

Project description:The A375, human BRAFV600E mutant melanoma, cell line (wildtype), two PTEN-null, BRAFV600E cell lines (KO5 and KO11), and PI3K overexpression cells (WT and PI3K H1047R mutant) were treated with small molecule inhibitors (dabrafenib, BRAF inhibitor; trametinib, MEK inhibitor alone and in combination for 0, 1 and 7 days

2019-04-27 | GSE130396 | GEO

Analysis of Amino Acid Variants in Malignant Melanoma Cells Resistant to BRAF inhibition

Project description:Analysis of patient-specific nucleotide variants is a cornerstone of personalised medicine. Although only 2% of the genomic sequence is protein-coding, mutations occurring in these regions have the potential to influence protein structure and may have severe impact on disease aetiology. Of special importance are variants that affect modifiable amino acid residues, as protein modifications involved in signal transduction networks cannot be analysed by genomics. Proteogenomics enables analysis of proteomes in context of patient- or tissue-specific non-synonymous nucleotide variants. Here, we developed a proteogenomics workflow and applied it to study resistance to serine/threonine-protein kinase B-raf (BRAF) inhibitor (BRAFi) vemurafenib in malignant melanoma cell line A375. This approach resulted in high identification and quantification of non-synonymous nucleotide variants and (phospho)proteins. We integrated multi-omic datasets to reconstruct the perturbed signalling networks associated with BRAFi resistance and to predict drug therapies with the potential to disrupt BRAFi resistance mechanism in A375 cells. Notably, we showed that aurora kinase A (AURKA) inhibition is effective and specific against BRAFi resistant A375 cells. Furthermore, we investigated nucleotide variants that interfere with protein post-translational modification (PTM) status and potentially influence cell signalling. Mass spectrometry (MS) measurements confirmed variant-driven PTM changes in 12 proteins; among them was the runt-related transcription factor 1 (RUNX1) displaying a variant on a known phosphorylation site S(Ph)276L. We confirmed the loss of phosphorylation site by MS and demonstrated the impact of this variant on RUNX1 interactome.

2021-11-04 | PXD018305 | Pride

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