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NK92 cells and peripheral blood NK cells respond oppositely upon dasatinib treatment

ABSTRACT: NK92 cells and peripheral blood NK cells respond oppositely upon dasatinib treatment

PROVIDER: PRJNA1027440 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26372085_1.fastq.gz	Fastqsanger.gz
	SRR26372085_2.fastq.gz	Fastqsanger.gz
	SRR26372086_1.fastq.gz	Fastqsanger.gz
	SRR26372086_2.fastq.gz	Fastqsanger.gz
	SRR26372087_1.fastq.gz	Fastqsanger.gz

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NK92 cells and peripheral blood NK cells respond oppositely upon dasatinib treatment

Project description:Natural Killer (NK) cell is a valuable tool for immunotherapy in cancer treatment, both the cultured cell line NK92 and primary NK cells are widely studied and used in the research and clinical trials. Clinical observations witnessed the improvement of patients’ NK cells in terms of cell counts and cytotoxic activity upon dasatinib treatment, an approved drug against CML and Ph+ ALL. Several studies supported the clinical observations, yet others argued a detrimental effect of dasatinib on NK cells. Due to the complex conditions in different studies, the definite influence of dasatinib on NK92 and primary NK cells remains to be settled. Here, we used a well-defined in vitro system to evaluate the effects of dasatinib on NK92 cells and peripheral blood (PB)-NK cells. By coculturing NK cells with dasatinib to test the cell counts and target cell killing activities, we surprisingly found that the chemical influenced oppositely on these two types of NK cells. While dasatinib suppressed NK92 cell proliferation and cytotoxic activity, it improved PB-NK killing tumor cells. RNA-seq analysis further supported this finding, uncovering several proliferating and cytotoxic pathways were responding invertedly between them. Our results highlighted an intrinsic difference between NK92 and PB-NK cells and may build clues to understand how dasatinib interacts with NK cells in vivo.

2023-10-17 | GSE245219 | GEO

mRNA expression profiles in YT and NK92 cells

2014-01-21 | GSE53478 | GEO

miRNA expression profiles in YT and NK92 cells

2014-01-21 | GSE53476 | GEO

miRNA expression profiles in YT and NK92 cells

Project description:The miRNA expression profiles of of EBV-infected YT and NK92 cells are compared. YT cells have weaker expression of T-bet and IFNg than NK92 cells. It was found that the EBV-encoded miR-BART20-5p inhibits the expression of T-bet and IFNg in YT cells. Approximately 100 ng total RNAs from YT and NK92 cells were used as the input. The GeneChip miRNA 2.0 array from Affymetrix, including probes for 44 EBV-encoded miRNAs and 1105 human miRNAs, was used. The experiments were performed in the microarray core laboratory of National Health Research Institute, Taiwan.

2014-01-21 | E-GEOD-53476 | biostudies-arrayexpress

mRNA expression profiles in YT and NK92 cells

Project description:YT and NK92 cells are EBV-infected lymphoma cells of NK- cell origin. YT cells have weaker expression of T-bet and IFNg than NK92 cells. However, this data set shows that both cell lines have similar mRNA levels, implying post-transcriptional regulations. Affymetrix chips (Human Genome U133 plus 2.0) were used for a genome-wide screen of transcriptional profiles on YT and NK cells. Hybridization and washing of the arrays were done according to the GeneChipÂ® Expression Analysis Technical Manual from Affymetrix. The arrays were scanned with GenePix 4000B (Molecular Devices, Sunnyvale, CA.), and the data were extracted with Affymetrix Microarray suite (MAS) software.

2014-01-21 | E-GEOD-53478 | biostudies-arrayexpress

Time kinetics of gene expression in NK92 cells after Plasmodium falciparum-iRBC encounter

Project description:To study the effect of Plasmodium falciparum-infected erythrocytes on gene expression in NK92 cells, microarray analysis after 6, 12 and 24 hours of co-culture with either uRBC or iRBC was performed. The aim was to identify pathways in NK92 cells that are switched on after iRBC encounter in a time-dependent manner that will help to understand the mechanisms in innate immune defenses against Plasmodium falciparum infection. Variation in gene expression of NK92 cells was determined after 6, 12, and 24 hours of co-culture with either infected or uninfected RBC compared to timepoint 0 (start of co-culture, untreated control). All experiments were done in triplicate, that means that samples were collected in 3 different experiments (A, B, and C) each time after 0, 6, 12 and 24 hours of co-culture.

2011-11-12 | E-GEOD-26876 | biostudies-arrayexpress

Time kinetics of gene expression in NK92 cells after Plasmodium falciparum-iRBC encounter

2011-11-12 | GSE26876 | GEO

Gene expression profiles of dasatinib-resistant and dasatinib-sensitive pancreatic cancer cell lines

Project description:Gene profiles from three dasatinib-resistant and three dasatinib-sensitive pancreatic cancer cell lines were compared by microarray analysis.

2015-02-24 | GSE59357 | GEO

Gene expression profiles of dasatinib-resistant and dasatinib-sensitive pancreatic cancer cell lines

Project description:Gene profiles from three dasatinib-resistant and three dasatinib-sensitive pancreatic cancer cell lines were compared by microarray analysis. RNA from three dasatinib-resistant (MiaPaCa2, Panc1, SU8686) and three dasatinib-sensitive (Panc0504, Panc0403, Panc1005) pancreatic cancer cell lines were extracted. Biological triplicates were employed for each cell line. Complementary DNA microarray analysis was performed using Illumina Human HT-12 v4 BeadChip (Illumina, San Diego, CA) at the National University of Singapore Core Facility following the manufacturer’s instructions.

2015-02-24 | E-GEOD-59357 | biostudies-arrayexpress

Global gene expression profile of dasatinib-resistant RCH-ACV cells

Project description:Purpose: Several ALL subtypes have been described depending on their karyotype, cell type, immunophenotype and gene-expression profile. Recently, a novel ALL subtype has been described and is characterized by expression of the pre-B cell receptor (pre-BCR). Interestingly, half of the cases is associated with the chromosomal translocation t(1:19), coding for the chimeric fusion protein E2A-PBX1, which is present in about 5% of pediatric and adult ALL. Using preclinical models, we and other groups have shown very promising preclinical activity of dasatinib in pre-BCR+ ALL and early clinical evidence supports our observations. To study mechanism of acquired dasatinib resistance, we generated dasatinib-resistant pre-BCR+/E2A-PBX1+ cell lines through multiple passages in the presence of increasing drug concentrations. Whole transcriptome analysis of dasatinib-sensitive and resistant ALL cells were performed to detect systematically differentially expressed genes and enriched pathways involved in dasatinib resistance.

2018-09-18 | GSE97352 | GEO

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