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RNA-sequencing of murine B16F10 melanoma cells with IFNg and FK866, a Nampt inhibitor

ABSTRACT: RNA-sequencing of murine B16F10 melanoma cells with IFNg and FK866, a Nampt inhibitor

PROVIDER: PRJNA853383 | ENA |

REPOSITORIES: ENA

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RNA-sequencing of murine B16F10 melanoma cells with IFNg and FK866, a Nampt inhibitor

Project description:NAMPT is expressed in all cells during normal cell homeostasis. However, melanoma cells have a higher energetic demand and increase NAMPT expression. Our data show that IFNg signaling upregulates NAMPT in both human and mouse melanoma cells leading to increased cell growth and expression kinetics. The purpose of this experiment was to identify how IFNg inducible Nampt alters cell kinetics and we did this by treating melanoma cells with the combination of IFNg and FK866.

2023-07-01 | GSE207060 | GEO

Molecular sequelae of Nampt Inhibition in Human Multiple Myeloma cell line

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2012-11-05 | E-GEOD-35414 | biostudies-arrayexpress

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)

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Effect of BMP2 on B16F10 melanoma cells

Project description:BMP2 treatment significantly reduces growth of B16F10 melanoma spheroids. This experiment analyses the transcriptome changes in B16F10 cells treated with or without BMP2.

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Stat1-induced NAMPT sustains glycolysis to regulate gene expression in classically activated macrophages

Project description:Single Cell RNA Sequencing is used to profile in vivo responses by immune cells lacking the Nampt NRE1 region to melanoma challenge, finding multiple defects in macrophages and other myeloid APCs. We analyzed B16F10 melanoma tumor infiltrating immune cells from mice specifically lacking NRE1 in hematopoietic cells, finding inflammatory and metabolic defects in APC populations within tumors, correlating with trends toward defective control of malignant growth.

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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

The NAMPT inhibitor FK866 increases metformin sensitivity in pancreatic cancer cells

Project description:Pancreatic cancer (pancreatic ductal adenocarcinoma: PDAC) is one of the most aggressive neoplastic diseases. Metformin use was associated with reduced pancreatic cancer incidence or better survival in diabetics. Metformin has been shown to inhibit PDAC cells survival and growth in vitro and in vivo. However, clinical trials using metformin failed to decrease pancreatic cancer progression in patients, raising important questions about molecular mechanisms that protect tumor cells from the antineoplastic activities of metformin. We confirm that metformin acts through inhibition of mitochondrial complex I, decreasing the NAD+/NADH ratio and that NAD+/NADH homeostasis determines metformin sensitivity in several cancer cell lines. Metabolites that can restore the NAD+/NADH ratio turned PDAC cells resistant to metformin. In addition, metformin treatment of PDAC cell lines induced a compensatory NAMPT expression increasing the pool of cellular NAD+. The NAMPT inhibitor FK866 sensitized PDAC cells to the antiproliferative effects of metformin in vitro and decreased cellular NAD+ pool. Intriguingly, FK866 combined with metformin increased survival in mice bearing KP4 cells xenografts but not in mice with PANC1 xenografts. Transcriptome analysis revealed that the drug combination reactivated genes in the p53 pathway and oxidative stress providing new insights about the mechanisms leading to cancer cell death.

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RNAseq of B16F10 melanoma CD31+ cells

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The NAMPT inhibitor FK866 increases metformin sensitivity in pancreatic cancer cells

Project description:The NAMPT inhibitor FK866 increases metformin sensitivity in pancreatic cancer cells

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