Evidence map›Paper›PMID 22768255›Full record

ArticlePloS one2012

Nicotinamide phosphoribosyl transferase (Nampt) is required for de novo lipogenesis in tumor cells.

Sarah C Bowlby, Michael J Thomas, Ralph B D'Agostino, Steven J Kridel

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.4field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Targeting NADFrontiers in immunology · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. NAMPT reduction-induced NADAging cell · 2021
    Article
  13. NADSignal transduction and targeted therapy · 2021
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Sarah C BowlbyDepartment of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, North Carolina, United States of America.
Michael J Thomas
Ralph B D'Agostino
Steven J Kridel
Wake Forest University · US

Funding

Training Program in Cancer BiologyT32CA079448 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI KRIDEL, STEVEN J. · 2000 to 2014
$6.5M
Fatty acid synthase inhibitors and prostate cancerR01CA114104 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI KRIDEL, STEVEN J. · 2006 to 2010
$1.2M
NCI NIH HHS CA114104NCI NIH HHS R01 CA114104NCI NIH HHS T32 CA079448NCI NIH HHS T32 CA079448-10
6 · The paper itself

Abstract

Tumor cells have increased metabolic requirements to maintain rapid growth. In particular, a highly lipogenic phenotype is a hallmark of many tumor types, including prostate. Cancer cells also have increased turnover of nicotinamide adenine dinucleotide (NAD(+)), a coenzyme involved in multiple metabolic pathways. However, a specific role for NAD(+) in tumor cell lipogenesis has yet to be described. Our studies demonstrate a novel role for the NAD(+)-biosynthetic enzyme Nicotinamide phosphoribosyltransferase (Nampt) in maintaining de novo lipogenesis in prostate cancer (PCa) cells. Inhibition of Nampt reduces fatty acid and phospholipid synthesis. In particular, short chain saturated fatty acids and the phosphatidylcholine (PC) lipids into which these fatty acids are incorporated were specifically reduced by Nampt inhibition. Nampt blockade resulted in reduced ATP levels and concomitant activation of AMP-activated protein kinase (AMPK) and phosphorylation of acetyl-CoA carboxylase (ACC). In spite of this, pharmacological inhibition of AMPK was not sufficient to fully restore fatty acid synthesis. Rather, Nampt blockade also induced protein hyperacetylation in PC-3, DU145, and LNCaP cells, which correlated with the observed decreases in lipid synthesis. Moreover, the sirtuin inhibitor Sirtinol, and the simultaneous knockdown of SIRT1 and SIRT3, phenocopied the effects of Nampt inhibition on fatty acid synthesis. Altogether, these data reveal a novel role for Nampt in the regulation of de novo lipogenesis through the modulation of sirtuin activity in PCa cells.

Indexed as

LipogenesisAdenylate KinaseCell Line, TumorCell SurvivalCytokinesEnzyme ActivationFatty AcidsFemaleHumansMaleNADNicotinamide PhosphoribosyltransferasePhospholipidsSignal TransductionSirtuinsAdenylate KinaseCytokinesFatty AcidsNADNicotinamide Phosphoribosyltransferasenicotinamide phosphoribosyltransferase, humanPhospholipidsSirtuins

Identifiers

PMID22768255
PMCPMC3387004
OpenAlexW2023747218

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.