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RNA sequencing of preB-ALL NALM-6 cells with or without XIAP-knockdown, using prime-seq

ABSTRACT: In this study we performed molecular manipulation of XIAP in vivo using microRNA-30 flanked shRNA expression in cell lines models of r/r ALL. Interestingly, upon strong XIAP knockdown, r/r ALL cells were outcompeted in vivo, while intermediate knockdown sensitized cells to chemotherapy. Using prime-seq we wanted to characterized NALM-6 cells expressing different XIAP levels.

ORGANISM(S): Homo sapiens

PROVIDER: GSE184011 | GEO | 2021/09/15

REPOSITORIES: GEO

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RNA sequencing of preB-ALL NALM-6 cells with or without XIAP-knockdown, using prime-seq

Project description:RNA sequencing of preB-ALL NALM-6 cells with or without XIAP-knockdown, using prime-seq

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Stable XIAP knockdown in HCT116 colon cancer cells

Project description:X-linked inhibitor of apoptosis (XIAP) is the most potent endogenous caspase inhibitor preventing cell death via caspase-9, -7 and -3 (initiator and executioner caspase pathways). Using short hairpin RNA (shRNA) against XIAP, stably expressed in a parent HCT116 human colon cancer cell line, a series of clones have been developed. XIAP mRNA levels were established by RT-PCR, the four X (XIAP knockdown) clonal cell lines show 82-93% reduction in XIAP mRNA when compared to the four L (luciferase control) cell lines. Immunoblot analysis showed a 67-89% reduction in XIAP protein in X cell lines compared to L. RNA was analysed by microarray and XIAP knockdown was confirmed in 7 probe sets, there was no significant compensation of other IAP family members. XIAP knockdown induced a 2-fold increase in the basal level of apoptosis without modification of caspase 3/7 activity. Finally, XIAP knockdown sensitises cells to radiotherapy by 20%, to recombinant TRAIL by a 3-fold factor, and to paclitaxel and docetaxel by >2 fold factor. Future work should focus on targeted agents such as rhTRAIL in combination with strategies to down regulate XIAP. XIAP antisense is now in clinical development in oncology.

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Nalm 6 WT; Nalm6 BKO; Nalm 6 A hets

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Transcription profiling of mouse embryonic fibroblasts from XIAP -/- animals after TNFa stimulation

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RNAseq of pedriatic IBD and XIAP-deficient biopsy samples

Project description:Deficiency in the X-linked inhibitor of apoptosis protein (XIAP) is the cause for the X-linked lymphoproliferative syndrome 2 (XLP2). About one third of all patients suffers from severe and therapy refractory inflammatory bowel disease (IBD), but the exact pathogenesis remains undefined. We examined the differences in gene expression of pediatric XLP2 patients with IBD to healthy controls and pediatric IBD patients.

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miR-515-5p suppresses trophoblast cell invasion and proliferation through XIAP regulation in preeclampsia

Project description:MicroRNAs (miRNAs) are non-coding small RNA molecules that can be secreted into the circulation and which exist in remarkably stable forms. Circulating miRNAs regulates numerous regulations of biological process and aberrantly expressed in pathological status. Differentially expressed circulating miRNAs have received attention as potential biomarkers for many diseases. In this study, we revealed that miR-515-5p was significantly upregulated in maternal serum from preeclampsia (PE) patients in comparison to normal pregnant women. Bioinformatics prediction and a dual-luciferase reporter gene assay revealed that miR-515-5p directly targets the X-linked inhibitor of apoptosis protein (XIAP) 3’-untranslated region (UTR). Furthermore, the XIAP mRNA expression was decreased in the preeclamptic placenta in comparison to that in normal pregnancy. The overexpression of miR-515-5p inhibited the proliferation and invasion of HTR-8/SVneo trophoblast cells. Collectively, miR-515-5p may play critical roles in the pathogenesis of PE through suppression of the expression of XIAP and serum miR-515-5p may act as a potential biomarker for PE

2022-06-26 | GSE206763 | GEO

MicroRNA profiling of human precursor B-cell acute lymphoblastic leukemia cell line NALM-6 after trichostatin A treatment

Project description:Expression profile of miRNAs in NALM-6 cells were analyzed after TSA treatment for 6h, compared with non-treated cells.

2009-11-06 | E-MEXP-2047 | biostudies-arrayexpress

TNFR2 induced priming of the inflammasome leads to a RIPK1-dependent cell death in the absence of XIAP

Project description:The pediatric immune deficiency X-linked proliferative disease-2 (XLP-2) is a unique disease, with patients presenting with either hemophagocytic lymphohistiocytosis (HLH) or intestinal bowel disease (IBD). Interestingly, XLP-2 patients display high levels of IL-18 in the serum even while in stable condition, presumably through spontaneous inflammasome activation. Recent data suggests that LPS stimulation can trigger inflammasome activation through a TNFR2/TNF/TNFR1 mediated loop in xiap−/− macrophages. Yet, the direct role TNFR2-specific activation plays in the absence of XIAP is unknown. We found TNFR2-specific activation leads to cell death in xiap−/− myeloid cells, particularly in the absence of the RING domain. RIPK1 kinase activity downstream of TNFR2 resulted in a TNF/TNFR1 cell death, independent of necroptosis. TNFR2-specific activation leads to a similar inflammatory NF-kB driven transcriptional profile as TNFR1 activation with the exception of upregulation of NLRP3 and caspase-11. Activation and upregulation of the canonical inflammasome upon loss of XIAP was mediated by RIPK1 kinase activity and ROS production. While both the inhibition of RIPK1 kinase activity and ROS production reduced cell death, as well as release of IL-1β, the release of IL-18 was not reduced to basal levels. This study supports targeting TNFR2 specifically to reduce IL-18 release in XLP-2 patients and to reduce priming of the inflammasome components.

2021-03-01 | E-MTAB-10103 | biostudies-arrayexpress

Enhancer profiling using H3K27Ac ChIP-seq signals in Kasumi-7, Kasumi-9, NAGL-1, and NALM-1 cell lines

Project description:Kasumi-7, Kasumi-9, NAGL-1, and NALM-1 cell lines were subjected to ChIP-seq analysis using anti-H3K27Ac antibody. Input signal reads are also provided.

2020-06-30 | E-MTAB-8463 | biostudies-arrayexpress

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