Cloning and characterization of the cDNA encoding a novel human pre-B-cell colony-enhancing factor.

Samal, Babru; Sun, Yinghao; Stearns, George; Xie, Chunshan; Suggs, Sid; McNiece, Ian

doi:10.1128/mcb.14.2.1431

Cited by 900 publications

(834 citation statements)

References 32 publications

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“…The specificity of the NAMPT antibody was validated as detailed in the methods and Supplementary Figure 2. NAMPT was expressed in certain normal tissues with the highest level in liver, pancreas, adrenal gland and muscle (Supplementary Figure 3A), consistent with previous reports (Samal et al, 1994;Fukuhara et al, 2005). We found that NAMPT expression was upregulated in many cancer types including prostate, colon, brain and lung cancer, as well as lymphoma when compared with their normal counterparts, with prostate exhibiting the most consistent and striking difference between normal tissue and cancer in arrays obtained from different sources (Figure 1c and Supplementary Figure 3B).…”

Section: Nampt Is Overexpressed In Human Prostate Cancersupporting

confidence: 92%

“…In mammals, NAD þ can be biosynthesized from nicotinamide (NAM), nicotinic acid or tryptophan, with NAM as the primary precursor (Garten et al, 2009). The rate limiting step for NAD þ biosynthesis from NAM is the transfer of a phosphoribosyl group to NAM, which is catalyzed by nicotinamide phosphoribosyltransferase (NAMPT) (Revollo et al, 2004), also known as pre-B-cell colony enhancing factor (Samal et al, 1994). NAMPT has a crucial role for growth factor-induced myeloid differentiation (Skokowa et al, 2009), circadian clock (Nakahata et al, 2009;Ramsey et al, 2009), glucose-restriction-impaired skeletal myoblast differentiation (Fulco et al, 2008) and insulin secretion in pancreatic beta cells (Revollo et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

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NAMPT overexpression in prostate cancer and its contribution to tumor cell survival and stress response

et al. 2010

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Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in regenerating nicotinamide adenine dinucleotide (NAD þ ) from nicotinamide in mammals. NAMPT has crucial roles for many cellular functions by regulating NAD þ -dependent SIRT1 deacetylase. However, roles of NAMPT in cancer are poorly defined. In this study, we show that NAMPT is prominently overexpressed in human prostate cancer cells along with SIRT1. Elevation of NAMPT expression occurs early for the prostate neoplasia. Inhibition of NAMPT significantly suppresses cell growth in culture, soft agar colony formation, cell invasion and growth of xenografted prostate cancer cells in mice. NAMPT knockdown sensitizes prostate cancer cells to oxidative stress caused by H 2 O 2 or chemotherapeutic treatment. Overexpression of NAMPT increases prostate cancer cell resistance to oxidative stress, which is partially blocked by SIRT1 knockdown. We demonstrate that in addition to modulating SIRT1 functions, the NAMPT inhibition reduces forkhead box, class 'O' (FOXO)3a protein expression and its downstream anti-oxidant genes catalase and manganese superoxide dismutase. Our results suggest important roles of concomitant upregulation of NAMPT and SIRT1 along with increased FOXO3a protein level for prostate carcinogenesis and their contribution to oxidative stress resistance of prostate cancer cells. These findings may have implications for exploring the NAMPT pathway for prostate cancer prevention and treatment.

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Section: Nampt Is Overexpressed In Human Prostate Cancersupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

NAMPT overexpression in prostate cancer and its contribution to tumor cell survival and stress response

et al. 2010

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“…Although the PBEF protein lacks a classic signal sequence for secretion, it is constitutively released and detected in conditioned medium from many cell types (12,13,(33)(34)(35)(36)(37). PBEF is detectable in serum and synovial fluid (1,6), and the levels of PBEF have been found to be increased in patients with rheumatoid arthritis, in whom it is clinically correlated with the Disease Activity Score in 28 joints and elevated C-reactive protein level (1,2,6).…”

Section: Discussionmentioning

confidence: 99%

Suppression of leukocyte infiltration and cartilage degradation by selective inhibition of pre-B cell colony-enhancing factor/visfatin/nicotinamide phosphoribosyltransferase: Apo866-mediated therapy in human fibroblasts and murine collagen-induced arthrit

Evans

Williams

Hayes

et al. 2011

Arthritis & Rheumatism

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Objective. To assess the ability of pre-B cell colony-enhancing factor (PBEF) to regulate inflammation and degradative processes in inflammatory arthritis, using the small molecule inhibitor APO866 in human fibroblasts in vitro and in murine collageninduced arthritis (CIA).Methods. Enzyme-linked immunosorbent assays were used to examine regulation of expression of metalloproteinases and chemokines in human fibroblasts. The role of PBEF was further examined using APO866 in mice with CIA, with effects on disease activity assessed using radiography, histology, in vivo imaging, and quantitative polymerase chain reaction (qPCR).Results. In vitro activation of human fibroblasts with PBEF promoted expression of matrix metalloproteinase 3 (MMP-3), CCL2, and CXCL8, an effect inhibited by APO866. In mice with CIA, early intervention with APO866 inhibited synovial inflammation, including chemokine-directed leukocyte infiltration, and reduced a systemic marker of inflammation, serum hyaluronic acid. APO866 blockade led to reduced expression of MMP-3 and MMP-13 in joint extracts and to a reduction in a systemic marker of cartilage erosion, serum cartilage oligomeric matrix protein. Radiologic images revealed that APO866 protected against bone erosion, while qPCR demonstrated inhibition of RANKL expression. In mice with established disease, APO866 reduced synovial inflammation and cartilage destruction, and halted bone erosion. In addition, APO866 reduced the activity of MMP-3, CCL2, and RANKL in vivo, and inhibited production of CCL2 and RANKL in synovial explants from arthritic mice, a result that was reversed with nicotinamide mononucleotide.Conclusion. These findings confirm PBEF to be an important regulator of inflammation, cartilage catabolism, and bone erosion, and highlight APO866 as a promising therapeutic agent for targeting PBEF activity in inflammatory arthritis.Pre-B cell colony-enhancing factor (PBEF) represents an inflammatory mediator that exerts enzymatic activities and is highly expressed within the synovial tissue and plasma of patients with rheumatoid arthritis (1,2). In this respect, PBEF acts as a nicotinamide phosphoribosyltransferase (referred to as NAMPT) that controls NAD biosynthesis by catalyzing nicotinamide with 5-phosphoribosyl-1-pyrophosphate (3-5). Conversely, exogenous PBEF is also described as an adipocytokine (referred to as visfatin), and can regulate cellular processes via activation of transcriptional events through NF-B, phosphatidylinositol 3-kinase, and MAP kinase (6-8). Several groups have shown that PBEF interacts with the insulin receptor (8-10); however, this notion remains controversial (11,12), and it may be that PBEF signals through an alternative signaling route. It is also unlikely that this signaling effect is attributable to the endotoxin that may be present in PBEF preparations, since coincubation with polymixin B shows no abrogation of PBEF signaling (6,10,13).In vitro activation of signaling pathways by PBEF has been shown to regulate the expression of metalloproteinases...

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“…Although PBEF has been regarded as an adipose tissue-related hormone, studies show that PBEF is ubiquitously expressed in the body. Among different human tissues, the maximum gene expression was found in the liver and peripheral blood leukocytes [6,22]. A large-scale analysis of the human transcriptome indicated that the PBEF gene is highly expressed in whole blood, over 100 times of the median abundance, while the expression in adipocytes is just about 2 times of the median abundance (GEO series GSE1133) [23].…”

Section: Discussionmentioning

confidence: 99%

“…Visfatin is a rediscovery of the cytokine-like protein pre-B cell colony-enhancing factor 1 (PBEF 1 ) [6]. It was also identified as cytosolic nicotinamide phosphoribosyltransferase (NAMPT), demonstrated by in vitro, in vivo, and structural studies [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

The circulating PBEF/NAMPT/visfatin level is associated with a beneficial blood lipid profile

Wang

Greevenbroek

Bouwman

et al. 2007

Pflugers Arch - Eur J Physiol

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Visfatin with the official gene name pre-B cell colony-enhancing factor 1 (PBEF) and the protein name nicotinamide phosphoribosyltransferase (NAMPT) is a recently discovered adipocyte-secreted protein that was shown by some to be associated with visceral fat and insulin resistance. To explore the link between PBEF/ NAMPT/visfatin and lipid metabolism, we analyzed the relation of its plasma level with several parameters of adiposity, insulin resistance and the circulating blood lipid profile in a group of general population (n=40) and a group of subjects who are genetically predisposed to insulin resistance and hyperlipidemia (n=35). In both groups and pooled cohort, PBEF/NAMPT/visfatin lacked association with whole body adiposity, but correlated positively with HDL-cholesterol and negatively with triglycerides. The data suggested a negative correlation of the PBEF level with visceral fat and insulin resistance. But this negative correlation completely disappeared after adjustment for lipid profile. We concluded that circulating PBEF/NAMPT/ visfatin level is an indicator of beneficial lipid profile in non-diabetic Caucasian subjects. The relation to lipid metabolism does not depend on visceral obesity and insulin resistance, but may be linked to its enzymatic function in NAD metabolism.

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Cloning and characterization of the cDNA encoding a novel human pre-B-cell colony-enhancing factor.

Abstract: A novel gene coding for the pre-B-cell colony-enhancing factor (PBEF)

Cited by 900 publications

References 32 publications

NAMPT overexpression in prostate cancer and its contribution to tumor cell survival and stress response

NAMPT overexpression in prostate cancer and its contribution to tumor cell survival and stress response

Suppression of leukocyte infiltration and cartilage degradation by selective inhibition of pre-B cell colony-enhancing factor/visfatin/nicotinamide phosphoribosyltransferase: Apo866-mediated therapy in human fibroblasts and murine collagen-induced arthrit

The circulating PBEF/NAMPT/visfatin level is associated with a beneficial blood lipid profile

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