Evidence map›Paper›PMID 18755846›Full record

ArticleThe American journal of pathology2008

Nitric oxide regulates tumor cell cross-talk with stromal cells in the tumor microenvironment of the liver.

Ningling Kang Decker, Soha S Abdelmoneim, Usman Yaqoob, Helen Hendrickson, Joe Hormes, Mike Bentley, Henry Pitot, Raul Urrutia, Greg J Gores, Vijay H Shah

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  3. Review
  4. Protein diaphanous homolog 1 (Diaph1) promotes myofibroblastic activation of hepatic stellate cells by regulating Rab5a activity and TGFβ receptor endocytosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  5. Article
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  7. Alterations of tumor microenvironment by nitric oxide impedes castration-resistant prostate cancer growth.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
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  10. Review
  11. Article
  12. Article
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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

10 authors at 4 institutions in 1 country.

Ningling Kang DeckerDepartment of Physiology, Mayo Clinic Rochester, MN 55905, USA. decker.ningling@mayo.edu
Soha S Abdelmoneim
Usman Yaqoob
Helen Hendrickson
Joe Hormes
Mike Bentley
Henry Pitot
Raul Urrutia
Greg J Gores
Vijay H Shah
Mayo Clinic · USMayo Clinic in Florida · USMinnesota State University, Mankato · USUniversity of Wisconsin–Madison · US

Funding

Tissue CoreP50CA102701 · NCI · MAYO CLINIC ROCHESTER · PI BILLADEAU, DANIEL D, PETERSEN, GLORIA M. · 2004 to 2018
$32.7M
ZINC FINGER GENES AND PANCREATIC CELL GROWTHR01DK052913 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI LOMBERK, GWEN, URRUTIA, RAUL A. · 1998 to 2023
$7.0M
Molecular Mechanisms of Portal HypertensionR01DK059615 · NIDDK · MAYO CLINIC ROCHESTER · PI SHAH, VIJAY H. · 2002 to 2023
$6.4M
Mechanisms of Nitric Oxide Signaling in Vascular RemodelingR01HL086990 · NHLBI · MAYO CLINIC ROCHESTER · PI SHAH, VIJAY H. · 2008 to 2011
$1.5M
Mechanism of nitric oxide inhibition of pericyte recruitment in liver tumorsK01CA118722 · NCI · MAYO CLINIC ROCHESTER · PI KANG, NINGLING · 2007 to 2011
$681k
NCI NIH HHS K01 CA118722NCI NIH HHS K01 CA118722-01A1NCI NIH HHS P50 CA102701NHLBI NIH HHS R01 HL086990NHLBI NIH HHS R01 HL86990NIDDK NIH HHS R01 DK052913NIDDK NIH HHS R01 DK059615
6 · The paper itself

Abstract

Tumor progression is regulated through paracrine interactions between tumor cells and stromal cells in the microenvironment, including endothelial cells and myofibroblasts. Nitric oxide (NO) is a key molecule in the regulation of tumor-microenvironment interactions, although its precise role is incompletely defined. By using complementary in vitro and in vivo approaches, we studied the effect of endothelial NO synthase (eNOS)-derived NO on liver tumor growth and metastasis in relation to adjacent stromal myofibroblasts and matrix because liver tumors maintain a rich, vascular stromal network enriched with phenotypically heterogeneous myofibroblasts. Mice with an eNOS deficiency developed liver tumors more frequently in response to carcinogens compared with control animals. In a surgical model of pancreatic cancer liver metastasis, eNOS overexpression in the tumor microenvironment attenuated both the number and size of tumor implants. NO promoted anoikis of tumor cells in vitro and limited their invasive capacity. Because tumor cell anoikis and invasion are both regulated by myofibroblast-derived matrix, we explored the effect of NO on tumor cell protease expression. Both microarray and Western blot analysis revealed eNOS-dependent down-regulation of the matrix protease cathepsin B within tumor cells, and silencing of cathepsin B attenuated tumor cell invasive capacity in a similar manner to that observed with eNOS overexpression. Thus, a NO gradient within the tumor microenvironment influences tumor progression through orchestrated molecular interactions between tumor cells and stroma.

Indexed as

AnimalsAnimals, Genetically ModifiedAnoikisAntigens, Polyomavirus TransformingCathepsin BCell Line, TumorDown-RegulationFemaleHumansLiver NeoplasmsMiceMice, SCIDModels, BiologicalNeoplasm MetastasisNitric OxideNitric Oxide Synthase Type IIIAntigens, Polyomavirus TransformingCathepsin BNitric OxideNitric Oxide Synthase Type III

Identifiers

PMID18755846
PMCPMC2543069
OpenAlexW1989575720

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.