Evidence map›Paper›PMID 16060857›Full record

ArticleThe Biochemical journal2005

Neutrophil gelatinase-associated lipocalin as a survival factor.

Zhimin Tong, Xuli Wu, Dmitriy Ovcharenko, Jiuxiang Zhu, Ching-Shih Chen, James P Kehrer

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

81 citing papers in PubMed, 185 citations in OpenAlex.

  1. Review
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  10. Cellular and Exosomal Regulations of Sepsis-Induced Metabolic Alterations.International journal of molecular sciences · 2021
    Review
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  17. Observational
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21 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Zhimin TongDivision of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, TX, USA. zhimin@mail.utexas.edu
Xuli Wu
Dmitriy Ovcharenko
Jiuxiang Zhu
Ching-Shih Chen
James P Kehrer
Austin College · USThe Ohio State University · US

Funding

Pilot Project ProgramP30ES007784 · NIEHS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI RICHIE, ELLEN R · 1996 to 2011
$16.4M
APOPTOSIS,5 LIPOXYGENASE ACTIVATING PROTEIN AND BCL XR01CA083701 · NCI · UNIVERSITY OF TEXAS AUSTIN · PI KEHRER, JAMES P · 2000 to 2004
$1.3M
Apoptosis Regulation by Lipid Signals in Prostate CancerR01CA094829 · NCI · OHIO STATE UNIVERSITY · PI CHEN, CHING-SHIH · 2001 to 2005
$995k
NCI NIH HHS CA83701NCI NIH HHS CA94829NCI NIH HHS R01 CA083701NCI NIH HHS R01 CA094829NIEHS NIH HHS ES07784NIEHS NIH HHS P30 ES007784
6 · The paper itself

Abstract

NGAL (human neutrophil gelatinase-associated lipocalin) and its mouse analogue 24p3 are members of the lipocalin family of small secreted proteins. These proteins are up-regulated in a number of pathological conditions, including cancers, and may function as transporters of essential factors. Although previous publications have suggested that 24p3 has pro-apoptotic functions, other data are more suggestive of a survival function. The current study was designed to determine whether NGAL is pro- or anti-apoptotic. Apoptosis induced in human adenocarcinoma A549 cells by the 5-lipoxygenase-activating-protein inhibitor MK886, or several celecoxib-derived PDK1 (phosphoinositide-dependent kinase 1) inhibitors that are devoid of cyclo-oxygenase-2 inhibitory activity, was accompanied by a dose- and time-dependent increase of NGAL mRNA levels, as was reported previously with 24p3. A similar induction of NGAL mRNA was observed in human breast cancer MCF7 cells treated with MK886, indicating this was not a cell-specific effect. Treatment of A549 cells with up to 150 mug/10(6) cells of purified recombinant NGAL protein had no effect on viability, whereas antisera against the full-length NGAL protein induced apoptosis in these cells. The stable overexpression of NGAL in A549 cells had no effect on proliferation or viability. However, the cell death induced by a PDK1 inhibitor was reduced by 50% in NGAL-overexpressing cells. Decreasing NGAL mRNA and protein expression with siRNA (small interfering RNA) in A549 cells increased the toxicity of a PDK1 inhibitor by approx. 45%. These data indicate that, although the induction of NGAL correlates with apoptosis, this induction represents a survival response. Because NGAL is a secreted protein, it may play an extracellular role in cell defence against toxicants and/or facilitate the survival of the remaining cells.

Indexed as

Apoptosis3-Phosphoinositide-Dependent Protein KinasesAcute-Phase ProteinsCell Line, TumorCell SurvivalChlorobenzenesDown-RegulationGene Expression RegulationHumansIndolesLipocalin-2LipocalinsProtein Serine-Threonine KinasesProto-Oncogene ProteinsPyrazolesRNA, Messenger3-Phosphoinositide-Dependent Protein KinasesAcute-Phase ProteinsChlorobenzenesIndolesLCN2 protein, humanLipocalin-2LipocalinsMK-886OSU 03012PDPK1 protein, humanPdpk1 protein, mouseProtein Serine-Threonine KinasesProto-Oncogene ProteinsPyrazolesRNA, MessengerSulfonamides

Identifiers

PMID16060857
PMCPMC1276944
OpenAlexW2006674808

What OpenQuestion holds

Textmetadata
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.