Natural Killer (NK) cells are primary effectors of innate immunity directed against transformed cells. In response, tumor cells have developed mechanisms to evade NK cell-mediated lysis but the molecular basis for target cell resistance is not well understood. In the present study, we used a lentiviral shRNA library targeting more than 1000 human genes to identify 83 genes that promote target cell resistance to human NK cells. Many of the genes identified in this genetic screen belong to common signaling pathways, however, none of these genes have previously been known to modulate susceptibility of human tumor cells to immunologic destruction. In particular, gene silencing of two members of the JAK family (JAK1 and JAK2) in a variety of tumor cell targets increased their susceptibility to NK-mediated lysis and induced increased secretion of interferon gamma (IFN-gamma by NK cells. Treatment of tumor cells with JAK inhibitors also induced increased susceptibility to NK cell activity. These findings may have important clinical implications and suggest that small molecule inhibitors of tyrosine kinases being developed as therapeutic anti-tumor agents may also have significant immunologic effects in vivo.
Tyrosine kinase pathways modulate tumor susceptibility to natural killer cells.
Cell line
View SamplesRNA-Seq was used to profile transcriptional changes induced by overexpression of the long non-coding RNA SLNCR1, as well as mutant version SLNCR1 delta conserved and SLNCR1 conserved. Overall design: The A375 melanoma cell line was transfected with pcDNA3.1 (-) expressing either full length SLNCR1, SLNCR1 delta conserved, or SLNCR1 conserved.
The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.
No sample metadata fields
View SamplesRNA-Seq was used to profile transcriptional changes induced by siRNA knockdown of the long non-coding RNA SLNCR1. Overall design: The WM1976 melanoma short-term culture was transfected with either scrambled or SLNCR1-targeting siRNAs
The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.
No sample metadata fields
View SamplesXenograft ovarian tumors are useful model to test therapeutic candidates in vivo. We used microarrays to gain insight into the expression changes during tumor growth and induced by the vitamin D analog, MT19C at multiple time points.
Integrated genomics of ovarian xenograft tumor progression and chemotherapy response.
Specimen part, Cell line, Treatment
View SamplesIn this study, by microarray we analyzed gene expression changes due to LMP1 signaling in B cells, in order to identify candidate co-stimulatory ligands that may account for the ability of LMP1-B cells to induce cytotoxic CD4+ T cell response. The identified candidate co-stimulatory ligands were further validated by other functional assays.
Signaling by the Epstein-Barr virus LMP1 protein induces potent cytotoxic CD4<sup>+</sup> and CD8<sup>+</sup> T cell responses.
Sex, Specimen part
View SamplesEffect of LUBEL catalytic dead mutation in immune response Overall design: Mutation was introduced in the LUBEL catalytic region by CRISPR/Cas9 techonology in Drosophila melanogaster and their transcriptome was compared in control (sample 23930 to 23941) and e.coli pricked samples (sample 28984 to 28995).
Linear ubiquitination by LUBEL has a role in Drosophila heat stress response.
Sex, Specimen part, Subject
View SamplesEffect of LUBEL catalytic dead mutation upon Heastshock Overall design: Mutation was introduced in CG11321 catalytic region by CRISPR/Cas9 techonology in Drosophila melanogaster and transcriptome was compared in untreated and heatshocked samples
Linear ubiquitination by LUBEL has a role in Drosophila heat stress response.
Treatment, Subject
View SamplesGLP-1 agonists are potent glucose-lowering agents, however, their effect on adolescent organisms needs to be clarified
Effects of the glucagon-like peptide-1 receptor agonist liraglutide in juvenile transgenic pigs modeling a pre-diabetic condition.
Age, Specimen part, Treatment
View SamplesIncreasing evidence across malignancies suggests that infiltrating T cells at the site of disease are crucial to tumor control. We hypothesized that marrow-infiltrating immune populations play a critical role in response to donor lymphocyte infusion (DLI), an established and potentially curative immune therapy whose precise mechanism remains unknown. We therefore analyzed marrow-infiltrating immune populations in 29 patients (22 responders, 7 nonresponders) with relapsed chronic myelogenous leukemia who received CD4+ DLI in the pre-tyrosine kinase inhibitor era.
Reversal of in situ T-cell exhaustion during effective human antileukemia responses to donor lymphocyte infusion.
Specimen part, Subject
View SamplesBackground: We got interested whether genes of airway basal cells are enriched in COPD.
BAL Cell Gene Expression Is Indicative of Outcome and Airway Basal Cell Involvement in Idiopathic Pulmonary Fibrosis.
Specimen part, Disease
View Samples