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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Molecular sequelae of Nampt Inhibition in Human Multiple Myeloma cell line

ABSTRACT: Evaluation of specific coordinated pattern of transcriptional events consistent with anti-myeloma activity of FK866 (chemical Nampt inhibitor) 3 samples were analyzed using as control the untreated cells. Treated cells were cultured in presence of FK866 at concentration of 10nM for 6 and 24 hours.

ORGANISM(S): Homo sapiens

SUBMITTER: Michele Cea

PROVIDER: E-GEOD-35414 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Targeting NAD+ salvage pathway induces autophagy in multiple myeloma cells via mTORC1 and extracellular signal-regulated kinase (ERK1/2) inhibition.

Cea Michele M Cagnetta Antonia A Fulciniti Mariateresa M Tai Yu-Tzu YT Hideshima Teru T Chauhan Dharminder D Roccaro Aldo A Sacco Antonio A Calimeri Teresa T Cottini Francesca F Jakubikova Jana J Kong Sun-Young SY Patrone Franco F Nencioni Alessio A Gobbi Marco M Richardson Paul P Munshi Nikhil N Anderson Kenneth C KC

Blood 20120905 17

Malignant cells have a higher nicotinamide adenine dinucleotide (NAD(+)) turnover rate than normal cells, making this biosynthetic pathway an attractive target for cancer treatment. Here we investigated the biologic role of a rate-limiting enzyme involved in NAD(+) synthesis, Nampt, in multiple myeloma (MM). Nampt-specific chemical inhibitor FK866 triggered cytotoxicity in MM cell lines and patient MM cells, but not normal donor as well as MM patients PBMCs. Importantly, FK866 in a dose-dependen ...[more]

PMID: 22955917

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Molecular sequelae of Nampt Inhibition in Human Multiple Myeloma cell line

Project description:Evaluation of specific coordinated pattern of transcriptional events consistent with anti-myeloma activity of FK866 (chemical Nampt inhibitor)

2012-11-05 | GSE35414 | GEO

Expression data from patients with advanced ovarian cancer

Project description:Integration of several ovarian cancer datasets to identify a reproducible predictors of survival Four microarray datasets from different institutions were reprocessed in a uniform manner, into a single training dataset. Survival analysis was performed and a validation cohort (61 patients from 3 institutions) was profiled using a custom array to confirm the prognostic value of the predictors. The four datasets were obtained from the following reports: Spentzos D, Levine DA, Ramoni MF, et al. Gene expression signature with independent prognostic significance in epithelial ovarian cancer. J Clin Oncol 2004;22:4700-10 Bild AH, Yao G, Chang JT, et al. Oncogenic pathway signatures in human cancers as a guide to targeted therapies. Nature 2006;439:353-7 Marquez RT, Baggerly KA, Patterson AP, et al. Patterns of gene expression in different histotypes of epithelial ovarian cancer correlate with those in normal fallopian tube, endometrium, and colon. Clin Cancer Res 2005;11:6116-26 Zhang L, Volinia S, Bonome T, et al. Genomic and epigenetic alterations deregulate microRNA expression in human epithelial ovarian cancer. Proc Natl Acad Sci U S A 2008;105:7004-9 61 samples

2011-06-15 | E-GEOD-19161 | biostudies-arrayexpress

The role of nicotinamide phosphoribosyltransferase (Nampt) in hippocampal neural stem/progenitor cells

Project description:Neural stem/progenitor cell (NSPC) proliferation and self-renewal, as well as insult-induced differentiation, decrease markedly with age, but the molecular mechanisms responsible for these declines remain unclear. Here we show that levels of NAD+ and nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in mammalian NAD+ biosynthesis, decrease with age in the hippocampus. Ablation of Nampt in adult NSPCs reduced their pool and proliferation in vivo. The decrease in the NSPC pool during aging can be rescued by enhancing hippocampal NAD+ levels. Nampt is the main source of NSPC NAD+ levels and required for G1/S progression of the NSPC cell cycle. Nampt is also critical for oligodendrocytic lineage fate decisions through a mechanism mediated redundantly by Sirt1 and Sirt2. Ablation of Nampt in the adult NSPCs in vivo reduced NSPC-mediated oligodendrogenesis upon injury. These phenotypes recapitulate defects in NSPCs during aging, implicating Nampt-mediated NAD+ biosynthesis as a mediator of these age-associated functional declines. Total RNA obtained from neurospheres derived from postnatal hippocampi subjected to 48 hours in vitro of incubation with Nampt-specific inhibitor FK866 (10 nM, 4 samples) or vehicle (DMSO, 1:1000, 4 samples).

2014-05-08 | E-GEOD-49784 | biostudies-arrayexpress

RNAi profiling of human MCF-7 cells depleted for NAMPT knockdown

Project description:NAMPT is an enzyme in the mammalian NAD+ salvage pathway. Expression microarray analysis was used to study the effect of NAMPT knockdown on gene expression in MCF-7 breast cancer cells. Experiment Overall Design: Stable knockdown of NAMPT was achieved using a retroviral shRNA construct. An shRNA directed against Luciferase was used to generate the Luc control cells. Three independent biological replicates with matching Luc controls were analyzed using Affymetrix U133 A2.0 microarrays.

2009-06-08 | E-GEOD-13449 | biostudies-arrayexpress

Identification differentially expressed genes upon valproic acid treatment

Project description:The goal of this study is to define genes that are differentially expressed in Down syndrome leukemic blasts after treatment with valproic acid (VPA) Here we report the identification gene sets that are downregulated in Down syndrome leukemic cell lines after exposure to valproic acid (VPA) CMK and CMY cells were treated with VPA for 24h and 48h with 1mM or 2mM VPA. Their gene expression profile was compared against the untreated control.

2011-07-12 | E-GEOD-30517 | biostudies-arrayexpress

Developmental stage-specific interplay between GATA1 and IGF signaling in fetal hematopoiesis and leukemogenesis

Project description:This SuperSeries is composed of the following subset Series: GSE16676: Rescue of murine Gata1s mutant M7 leukemic cells by full-length Gata1 GSE16677: Gene expression profiling of Down Syndrome (DS)-AMKL and non-DS AMKL samples GSE16679: Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia GSE16682: Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors GSE16684: Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors depends on IGF signaling Refer to individual Series

2010-08-01 | E-GEOD-16655 | biostudies-arrayexpress

Rescue of murine Gata1s mutant M7 leukemic cells by full-length Gata1

Project description:In this project, we studied a mouse model of human Down Syndrome (DS) megakaryocytic leukemia involving mutations in the GATA1 transcription factor (called GATA1s mutation). The model was generated through retroviral insertional mutagenesis in Gata1s mutant fetal liver progenitors. In this study, we analyzed the dependency of these leukemic cells on the Gata1s mutant protein. Here we report Gata1s mutant leukemic cells were dependent on this mutant protein. Introduction of the full-length Gata1 protein to these cells led to their reduced proliferation and increased differentiation along the megakaryocytic lineage. We transduced leukemic cells with Gata1/estrogen receptor fusion cDNA (Gata1-ER) and generated stable cell lines. Addition of beta-estradiol to culture medium led to activation of the full-length Gata1 protein in synchronized leukemic cells. Gene expression profiles were collected at multiple time points.

2010-08-01 | E-GEOD-16676 | biostudies-arrayexpress

Gene expression profiling of Down Syndrome (DS)-AMKL and non-DS AMKL samples

Project description:The goal of this study is to define a gene expression signature unique to DS-AMKL (acute megakaryoblastic leukemia or FAB M7 leukemia). A similar study was done previously, but using unfractionated patient leukemic samples. In this study, we sorted megakaryocytic leukemia blasts from patients and then compared their gene expression signatures to those from similarly sorted blasts from patients with non-DS AMKL. This allowed us to identify a gene expression signature more unique to DS-AMKL samples. The leukemic blasts were sorted based on CD41, CD7, CD117, CD33, and CD34 antibodies as previously described (Klin. Padiatr. 217, 126-134).

2010-08-01 | E-GEOD-16677 | biostudies-arrayexpress

Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia

Project description:The goal of this study is to develop a Plag1 signature and determine how its overexpression contributes to leukemogenesis. To study this, we transduced an immortalized (but not transformed) cell line (derived from Gata1s mutant fetal liver progenitor through insertional mutagenesis) by Plag1-expressing retrovirus. This turned a non-transformed cell line to a leukemogenic cell line. To study whether Plag1 overexpression led to deregulation of signaling pathways that may contribute to leukemic transformation, we generated microarray gene expression profiles of this cell line transduced with either Plag1 or the empty vector. We generated gene expression profiles by microarray from stable cell lines transduced with either the empty vector or the Plag1-expressing vector.

2010-08-01 | E-GEOD-16679 | biostudies-arrayexpress

Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors

Project description:The goal of this study is to derive a mouse model of human Down Syndrome (DS) megakaryocytic leukemia involving mutations in the hematopoietic transcription factor, GATA1 (called GATA1s mutation). We achieved this through transduction of Gata1s mutant fetal progenitors by MSCV-based retrovirus expressing a GFP marker, followed by in vitro selection (for immortalized cell lines), and then in vivo selection (for transformed cell lines) through transplantation. Here we report one such cell line [T6(6)] that gives rise to megakaryocytic leukemia (M7 leukemia) upon transplantation. Since the leukemic cells were retrovirally tagged with a GFP reporter, we sorted GFP+ leukemic blasts and generated their expression profiles by microarray.

2010-08-01 | E-GEOD-16682 | biostudies-arrayexpress

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