MiRNA expression profiles in YT and NK92 cells
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ABSTRACT:
ORGANISM(S): synthetic construct Homo sapiens
PROVIDER: GSE53476 | GEO | 2014/01/21
SECONDARY ACCESSION(S): PRJNA232713
REPOSITORIES: GEO
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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
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.
2014-01-21 | GSE53478 | GEO
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 GeneChip® 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
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
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.
2011-11-12 | GSE26876 | GEO
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
Project description:T-bet is a critical transcription factor for T helper 1 (Th1) cell differentiation. To study the regulation and functions of T-bet, we developed a T-bet-ZsGreen reporter mouse strain, in which GFP faithfully reflects the expression of T-bet. By using this tool, we report that signals elicited by IL-12 and IFNg are redundant in inducing T-bet in mice infected with Toxoplasma gondii and that T-bet does not contribute to its own expression when induced by IL-12 and IFNg. While both T-bet and Stat4 are critical for IFNg production, IFNg signaling is dispensable. Strikingly, loss of T-bet results in activation of an endogenous Th2 program in cells expressing T-bet-ZsGreen. Genome-wide analyses suggest T-bet directly induces Th1-related genes but indirectly suppresses Th2-related genes. Our study revealed redundancy and synergy among several Th1-inducing pathways in regulating the expression of T-bet and IFNg, and a critical role of T-bet in suppressing an endogenous Th2 program. RNA-Seq experiments were performed using total RNAs isolated from both wild type and Tbx21-/- Th1 cells in duplicates. Tbet ChIP-seq was performed using wild type Th1 cells. H3K4me1 and H3K27me3 ChIP-seq was performed using both wild type and Tbx21-/- Th1 cells.
2012-10-04 | E-GEOD-38808 | biostudies-arrayexpress
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are using mRNA and microRNA sequencing analysis to evaluate the effects of EBV-encoded microRNA BART2-5p mimics on the mRNA and microRNA profiles of human nasopharyngeal carcinoma cell line 6-10B. Methods: 6-10B cells were transfected with either EBV microRNA BART2-5p mimics or negative control (NC) mimics for 48 hours. Cellular RNA was then sequenced at the mRNA and microRNA levels using illumina high-throughput sequencing service (Oebiotech, Shanghai, China). Data were extracted and normalized according to the manufacturer's standard protocol. Results: Log-fold changes of up- or down-regulated mRNAs and microRNAs between the control and experiment group were selected with a significance threshold of p<0.05. Conclusions: Our study describes the mRNA and microRNA alterations induced by EBV-miRNA-BART2-5p in 6-10B cells
2023-09-14 | GSE220166 | GEO
Project description:CD25 (IL2RA) is a subunit of IL2 receptor complex, which determines the sensitivity of the receptor to IL2. Here, we investigated whether PRDM1, a transcriptional repressor implicated as a tumor suppressor in NK cell malignancies, directly represses CD25 (IL2RA). Using ChIP-seq, we identified a direct binding site of PRDM1 within 1st intron of CD25 (IL2RA) in activated primary human NK cells. We used DNA microarrays on two PRDM1α transduced NK cell lines (i.e. NK92 and KHYG1) to address whether PRDM1 transcriptionally represses CD25.
2021-05-05 | GSE157206 | GEO
Project description:T-bet is a critical transcription factor for T helper 1 (Th1) cell differentiation. To study the regulation and functions of T-bet, we developed a T-bet-ZsGreen reporter mouse strain, in which GFP faithfully reflects the expression of T-bet. By using this tool, we report that signals elicited by IL-12 and IFNg are redundant in inducing T-bet in mice infected with Toxoplasma gondii and that T-bet does not contribute to its own expression when induced by IL-12 and IFNg. While both T-bet and Stat4 are critical for IFNg production, IFNg signaling is dispensable. Strikingly, loss of T-bet results in activation of an endogenous Th2 program in cells expressing T-bet-ZsGreen. Genome-wide analyses suggest T-bet directly induces Th1-related genes but indirectly suppresses Th2-related genes. Our study revealed redundancy and synergy among several Th1-inducing pathways in regulating the expression of T-bet and IFNg, and a critical role of T-bet in suppressing an endogenous Th2 program.
2012-10-04 | GSE38808 | GEO