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Neural cell adhesion molecule 1 (NCAM1; CD56) promotes leukemogenesis and confers drug resistance in acute myeloid leukemia.

ABSTRACT: Neural cell adhesion molecule 1 (NCAM1; also known as CD56) is expressed in up to 20% of acute myeloid leukemia (AML) patients. Expression of NCAM1 is widely used as a marker of minimal residual disease; however, the biological function of this cell surface protein in AML remains elusive. In this study we investigated the impact of aberrant NCAM1 expression on leukemogenesis, drug resistance and its role as a biomarker to guide therapy.Gene expression profiling was performed with RNA-seq in three cell lines (SKM-1, NOMO-1, MOLM-14) after doxycycline-mediated induction of scrambled shRNA or shNCAM1 at timepoint 72 hours.

ORGANISM(S): Homo sapiens

PROVIDER: GSE123071 | GEO | 2019/02/22

REPOSITORIES: GEO

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Neural cell adhesion molecule 1 (NCAM1; CD56) promotes leukemogenesis and confers drug resistance in acute myeloid leukemia.

Project description:Neural cell adhesion molecule 1 (NCAM1; CD56) promotes leukemogenesis and confers drug resistance in acute myeloid leukemia.

| PRJNA507440 | ENA

Gene expression analysis for CD56- T, NK, CD56+ T cells, and iNKT cells

Project description:A small subset of T cells also expresses kiler-cell immunoglobulin-like receptors (KIRs). We find that KIR+ T cells primarily reside in the CD56+ T population. However, little is known on how these cells are different from the conventional CD56- T, NK, and iNKT cells. We used microarray profiling to compare and determine the distinctive differences of CD56+ T cell and its KIR subsets when compared to the conventional CD56- T, NK and iNKT cells. Lymphocyte subsets were sorted from human peripheral blood mononuclear cells with FACSAriaII (BD Biosciences, San Jose, CA) using anti-CD3, anti-CD56, anti-CD14, anti-KIR2DL1, anti-KIR2DL2/3, anti-KIR3DL1 and anti-TCRValpha24 antibodies. The purity of CD3+CD56- T cells, CD3-CD56+ NK cells, CD3+CD56+ T cells, KIR-CD3+CD56+ T cells, and KIR+CD3+CD56+ T cells were more than 98% in all experiments. The purities of iNKT cells for TCRValpha24 and CD1d-tetramer were >95% and >90%, respectively. RNA pre-amplification, labeling and hybridization on Human Genome U133Plus 2.0 GeneChip array were performed in the St. Jude Hartwell Center for Bioinformatics & Biotechnology microarray core facility according to the manufacturer’s instructions (Affymetrix, Santa Clara, CA).

2013-07-01 | E-GEOD-47855 | biostudies-arrayexpress

Gene expression analysis for CD56- T, NK, CD56+ T cells, and iNKT cells

2013-07-01 | GSE47855 | GEO

A Critical Role of Nuclear m6A Reader YTHDC1 in Leukemogenesis by Regulating MCM Complex-Mediated DNA Replication

Project description:PLKO.1 lentiviral vectors contained scramble shRNA, YTHDC1 shRNA 1# and YTHDC1 shRNA 2# were transfected into 293T cells together with package plasmids pMDG.2 and Δ8.91. The supernatant medium contained virus was collected and subjected to infect MOLM-13 cells by spinoculation, MOLM-13 cell is an AML cell line. The positive cells were collected 3 days after viral infection and subjected to RNA-seq.

2021-06-25 | GSE178859 | GEO

Human CD56+ ILC1-like cells

Project description:CD56 as a marker of an ILC1-like population with NK cell properties that is functionally impaired in AML

| PRJEB34980 | ENA

Isoform-specific regulation of NCAM1 gene expression in ischemic cardiomyopathy

Project description:Although ischemic cardiomyopathy (ICM) is the leading cause of chronic heart failure, one of the most common diseases overall, many aspects of the molecular pathogenesis of ICM still remain to be clarified. It has been We have previously shown that the neural cell adhesion molecule (NCAM1, CD56) is upregulated in ischemic cardiomyopathy by novel isoforms of the transcription factor RUNX1 (AML1) and, in the current study, we show that this upregulation is attributed exclusively to the NCAM1 isoform CD56-140kD. Moreover, we show that the upregulation of CD56-140kD has proapoptotic and antiproliferative effects on cardiomyocytes in vitro as well as inducing mitochondrial damage and reducing the capacity for Ca2+-uptake. As loss of cells and negative inotropy have previously been identified as major components in the development of ischemic cardiomyopathy, these data suggest that the upregulation of CD56-140kD may play a relevant role in the pathogenesis of ICM and therapeutic strategies targeting this molecule may prove to be valuable tools in the management of this very common and often fatal disease in the future.

2014-12-01 | GSE34124 | GEO

Kevetrin induces apoptosis in TP53 wild-type and mutant acute myeloid leukemia cells

Project description:Tumor protein p53 is a key regulator of several cellular pathways, including DNA repair, cell cycle and angiogenesis. Kevetrin exhibits p53-dependent as well as independent activity in solid tumors, while its effects on leukemic cells remain unknown. We analyzed the response of acute myeloid leukemia (AML) cell lines (TP53 wild-type: OCI-AML3 and MOLM-13; and TP53-mutant: KASUMI-1 and NOMO-1) to kevetrin at a concentration range of 85-340 μM. Kevetrin induced cell growth arrest and apoptosis in all cell lines and in primary cells, with TP53-mutant models displaying a higher sensitivity and p53 induction. Gene expression profiling revealed a common core transcriptional program altered by drug exposure and the downregulation of glycolysis, DNA repair and unfolded protein response signatures. These findings suggest that kevetrin may be a promising therapeutic option for patients with both wild-type and TP53-mutant AML.

2020-09-03 | GSE137574 | GEO

In vitro differentiated CD56-positive ILC transcriptional profiling via scRNA-seq

Project description:The innate cytotoxic Natural Killer (NK) cells emerged during hematopoiesis through a linear model of human NK development, yet how in vitro model of NK differentiation recapitulates in vivo process is largely under-explored. Here, we established that NK cell trajectory in vitro can be divided into 4 stages by sequential acquisition of CD161, CD56 and CD94 in which CD56 bifurcation can separate Stage 3a (CD56-) as ILC-precursor that can further give rise to stage 3b (CD56+) and stage 4 (CD94+). Re-plating results together with clonal tracing between S3b, S4 and ILC3 subsets supported a diverging developmental point between NK and ILC3 lineages occurs at the S3a stage and accompanied by the loss of the ILC3 potential as NK cell maturation progress from S3b toward S4. Single-cell transcriptomic and RNA-velocity connected the NK cytotoxic trajectory with a coordinated network of transcription factors (TFs) that are highly compatible with primary NK cell gene program.

2023-06-30 | GSE235708 | GEO

Immunophenotypic and detailed cytogenetic characterization of cell lines derived from myelodysplastic syndrome patients after progression to acute myeloid leukemia

Project description:Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from cultured cells. Five cell lines (MOLM-13, SKM-1, F-36P, SKK-1 and OHN-GM) derived from myelodysplastic syndrome patients after progression to acute myeloid leukemia have been studied by flow cytometry, conventional cytogenetics and whole genome single nucleotide polymorphism microarrays, in order to deeply characterize.

2017-01-01 | GSE80314 | GEO

Epigenome analysis of parental and ABT-199 resistant AML cell lines

Project description:Genome wide DNA methylation profiling of parental, ABT-199 resistant population, and ABT-199 resistant clones from 3 acute myelogenous leukemia (AML) cell lines (MOLM-13, MV-4-11, OCI-AMLO2). The Illumina Infinium MethylationEPIC Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpGs from AML cell line samples. Samples include 4 ABT-199 sensitive parental MOLM-13 population samples, 4 ABT-199 resistant MOLM-13 population samples, 3 ABT-199 resistant MOLM-13 S2 clone samples, 3 ABT-199 resistant MOLM-13 S5 clone samples, 4 ABT-199 resistant MOLM-13 S6 clone samples, 3 ABT-199 sensitive parental MV-4-11 population samples, 3 ABT-199 resistant MV-4-11 population samples, 3 ABT-199 sensitive parental OCI-AML2 population samples, 3 ABT-199 resistant OCI-AML2 population samples, 3 ABT-199 resistant OCI-AML2 S1 clone samples, 3 ABT-199 resistant OCI-AML2 S2 clone samples, 3 ABT-199 resistant OCI-AML2 S8 clone samples.

2022-01-12 | GSE193254 | GEO

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