CXXC Finger Protein 1 Is Required for Normal Proliferation and Differentiation of The PLB-985 Myeloid Cell Line

2007 ◽  
Vol 26 (2) ◽  
pp. 80-90 ◽  
Author(s):  
Suzanne R.L. Young ◽  
David G. Skalnik
Keyword(s):  
Cell Line ◽  
Myeloid Cell ◽  
Finger Protein ◽  
Proliferation And Differentiation ◽  
Myeloid Cell Line ◽  
Cxxc Finger Protein 1

AZT Incorporation into Mitochondria: Study in a Human Myeloid Cell Line

1996 ◽  
Vol 15 (5) ◽  
pp. 363-366 ◽  
Author(s):  
NEIL J. NUSBAUM ◽  
PHILLIP E. JOSEPH
Keyword(s):  
Cell Line ◽  
Myeloid Cell ◽  
Myeloid Cell Line

scholarly journals Detailed molecular cytogenetic characterisation of the myeloid cell line U937 reveals the fate of homologous chromosomes and shows that centromere capture is a feature of genome instability

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Ruth N. MacKinnon ◽  
Joanne Peverall ◽  
Lynda J. Campbell ◽  
Meaghan Wall
Keyword(s):  
Cell Line ◽  
Chromosome Pair ◽  
Fusion Gene ◽  
Genome Instability ◽  
Snp Array ◽  
Myeloid Cell ◽  
Chromosome 20 ◽  
Myeloid Cell Line ◽  
Multicolour Fish ◽  
Chromosome Segments

Abstract Background The U937 cell line is widely employed as a research tool. It has a complex karyotype. A PICALM-MLLT10 fusion gene formed by the recurrent t(10;11) translocation is present, and the myeloid common deleted region at 20q12 has been lost from its near-triploid karyotype. We carried out a detailed investigation of U937 genome reorganisation including the chromosome 20 rearrangements and other complex rearrangements. Results SNP array, G-banding and Multicolour FISH identified chromosome segments resulting from unbalanced and balanced rearrangements. The organisation of the abnormal chromosomes containing these segments was then reconstructed with the strategic use of targeted metaphase FISH. This provided more accurate karyotype information for the evolving karyotype. Rearrangements involving the homologues of a chromosome pair could be differentiated in most instances. Centromere capture was demonstrated in an abnormal chromosome containing parts of chromosomes 16 and 20 which were stabilised by joining to a short section of chromosome containing an 11 centromere. This adds to the growing number of examples of centromere capture, which to date have a high incidence in complex karyotypes where the centromeres of the rearranged chromosomes are identified. There were two normal copies of one chromosome 20 homologue, and complex rearrangement of the other homologue including loss of the 20q12 common deleted region. This confirmed the previously reported loss of heterozygosity of this region in U937, and defined the rearrangements giving rise to this loss. Conclusions Centromere capture, stabilising chromosomes pieced together from multiple segments, may be a common feature of complex karyotypes. However, it has only recently been recognised, as this requires deliberate identification of the centromeres of abnormal chromosomes. The approach presented here is invaluable for studying complex reorganised genomes such as those produced by chromothripsis, and provides a more complete picture than can be obtained by microarray, karyotyping or FISH studies alone. One major advantage of SNP arrays for this process is that the two homologues can usually be distinguished when there is more than one rearrangement of a chromosome pair. Tracking the fate of each homologue and of highly repetitive DNA regions such as centromeres helps build a picture of genome evolution. Centromere- and telomere-containing elements are important to deducing chromosome structure. This study confirms and highlights ongoing evolution in cultured cell lines.

The Leukemic Myeloid Cell Line OMA-AML-1: AnIn VitroModel of Hematopoietic Cell Differentiation

1994 ◽  
Vol 13 (1-2) ◽  
pp. 169-178 ◽  
Author(s):  
Samuel J. Pirruccello ◽  
John D. Jackson ◽  
J. Graham Sharp
Keyword(s):  
Cell Differentiation ◽  
Cell Line ◽  
Myeloid Cell ◽  
Hematopoietic Cell ◽  
Myeloid Cell Line

Cotreatment with Pioglitazone, a Synthetic Ligand for Peroxisome Proliferator-Activated Receptor γ (PPARγ), Enhances Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-Induced Apoptosis of Human Leukemia Cells.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4377-4377
Author(s):  
Joo-In Park ◽  
Hoon Han ◽  
Ji-Seon Han ◽  
Hyuk-Chan Kwon ◽  
Jin-Yeong Han ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cell Line ◽  
Myeloid Cell ◽  
Leukemia Cells ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Myeloid Cell Line ◽  
Synthetic Ligand ◽  
Induced Apoptosis ◽  
Acute Myeloid

Abstract Imatinib (STI571, Glivec) is the choice treatment for Bcr/Abl-positive malignancies. Emergence of resistance to Imatinib warrants the exploration of novel well-tolerated anticancer agents. Peroxisome proliferator-activated receptor γ (PPARγ) is a nuclear receptor family, which mainly associates with the adipocyte differentiation, but also appears to facilitate cell differentiation or apoptosis in certain malignant cells. Previous studies imply that the PPARγ activation pathway may be a possible intervention mode for treatment of leukemia, which is resistant to imatinib (STI571). In this study, we investigated the effects of pioglitazone, a synthetic ligand for PPARg, on the cell growth and TRAIL-induced apoptosis in a novel imatinib (STI571) resistant acute myeloid cell line (SR-1), which we have established from an STI571 resistant blast crisis patient, as well as HL-60 cells. HL-60 and SR-1 cells are relatively resistant to TRAIL-induced apoptosis. Pioglitazone alone inhibited the cell growth of SR-1 and HL-60 cells, but did not induce the apoptosis of these cell lines. However, simultaneous exposure of cells to 100 ng/ml TRAIL with either 25 μM pioglitazone or 50 μM piogliazone resulted in a striking increase in apoptosis. To clarify the mechanism of pioglitazone to sensitize the leukemia cells to TRAIL-induced apoptosis, we investigated the change of the proteins related to cell cycle and apoptosis by western blot. As results, we observed the significant decrease of X-linked inhibitor of apoptosis (XIAP) and the increased expression of p21 by cotreatment of pioglitazone with TRAIL. Taken together, these findings indicate that pioglitazone may have promising activity in augmenting TRAIL-induced apoptosis of human acute leukemia cells including the imatinib (STI571) resistant acute myeloid cell line.

mRNA and Protein Expression Levels of Secretory Leukocyte Protease Inhibitor (SLPI) Are Severely Reduced in Patients with Severe Congenital Neutropenia (CN)

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2165-2165
Author(s):  
Wienke Ellerbeck ◽  
Olga Klimenkova ◽  
Julia Skokowa ◽  
Karl Welte
Keyword(s):  
Protease Inhibitor ◽  
Cell Line ◽  
Myeloid Cells ◽  
Myeloid Cell ◽  
Myeloid Differentiation ◽  
Severe Congenital Neutropenia ◽  
Healthy Individuals ◽  
Congenital Neutropenia ◽  
Protein Levels ◽  
Myeloid Cell Line

Abstract Abstract 2165 Secretory Leukocyte Protease Inhibitor (SLPI) is a cationic serine protease inhibitor with antiprotease, primarily anti-Neutrophil ELastase (NE), activities. Moreover, SLPI modulates intracellular signal transduction pathways such as NF-kB and Erk. The molecular interaction and the balance between NE and SLPI is tightly regulated. On the one side, NE upregulates the SLPI expression and at the other hand SLPI inhibits the NE-induced degradation of proteins. We identified severe diminished levels of SLPI mRNA in CD33+ myeloid cells and in PMNs of patients with severe congenital neutropenia (CN) harbouring either ELANE or HAX1 mutations, as compared to patients with cyclic neutropenia (CyN) and to healthy individuals. SLPI protein levels in plasma of CN patients were also significantly reduced. We further analysed whether diminished levels of SLPI are associated with the „maturation arrest“ of myeloid cells seen in CN patients. We inhibited SLPI using lentivirus-based transduction of the myeloid cell line NB4 with SLPI-specific shRNA and analysed ATRA-triggered myeloid differentiation. Indeed, myeloid differentiation was severely affected in NB4 cells transduced with SLPI-specific shRNA, as compared to control shRNA transduced cells. Further, we analysed the mechanisms leading to SLPI downregulation. Previously, we identified severely reduced mRNA and protein levels of NE in myeloid cells and in plasma of CN patients with either ELANE or HAX1 mutations, as compared to healthy individuals. Knowing that NE induces SLPI expression, we assumed that diminished NE levels may be responsible for the low SLPI expression in CN patients. Indeed, inhibition of NE in the myeloid cell line NB4 using NE-specific shRNAs led to diminished expression of SLPI mRNA, as compared to ctrl shRNA transduced cells. At the same time, we also found that transduction of the myeloid cell line NB4 with wild type (WT) NE resulted in the increased expression of SLPI mRNA but mutated (MUT) forms of NE as found in CN patients were not able to induce SLPI mRNA, as compared to ctrl transduced cells. Taken together, both diminished NE levels and mutations in ELANE gene may cause downregulation of SLPI. In summary, SLPI is severely downregulated in CN patients due to defective NE protein levels and ELANE mutations. As a consequence, the anti-microbial and antiinflammatory activities of SLPI are diminished in CN patients. Disclosures: No relevant conflicts of interest to declare.

Malignant transformation of a growth factor-dependent myeloid cell line by Abelson virus without evidence of an autocrine mechanism

Cell ◽  
1985 ◽  
Vol 41 (3) ◽  
pp. 677-683 ◽  
Author(s):  
Wendy D. Cook ◽  
Donald Metcalf ◽  
Nicos A. Nicola ◽  
Antony W. Burgess ◽  
Francesca Walker
Keyword(s):  
Growth Factor ◽  
Cell Line ◽  
Malignant Transformation ◽  
Myeloid Cell ◽  
Myeloid Cell Line ◽  
Abelson Virus ◽  
Autocrine Mechanism
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