Evidence map›Paper›PMID 23555575›Full record

ArticlePloS one2013

Targeted deletion of the metastasis-associated phosphatase Ptp4a3 (PRL-3) suppresses murine colon cancer.

Mark W Zimmerman, Gregg E Homanics, John S Lazo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. 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
3.9field-weighted citation impact, top 6% 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, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. International journal of molecular sciences · 2023
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
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  13. Article
  14. Article
  15. Review
  16. Article
  17. Review of PIP2 in Cellular Signaling, Functions and Diseases.International journal of molecular sciences · 2020
    Review
  18. Article
  19. Article
  20. A chemical genetics approach identifies PTP4A3 as a regulator of colon cancer cell adhesion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    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

3 authors at 2 institutions in 1 country.

Mark W ZimmermanDepartment of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Gregg E Homanics
John S Lazo
University of Pittsburgh · USUniversity of Virginia · US

Funding

Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Thomas P. Loughran · 1987 to 2026
$72.1M
Ethanol Mechanisms in GABAAR Gene Targeted MiceR37AA010422 · NIAAA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HOMANICS, GREGG E. · 2010 to 2019
$4.4M
ETHANOL MECHANISMS IN GABAAR GENE TARGETED MICER01AA010422 · NIAAA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HOMANICS, GREGG E. · 1995 to 2008
$3.1M
The Role of Phosphatase of Regenerating Liver-3 in Alcohol-Associated DiseaseF31AA019597 · NIAAA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZIMMERMAN, MARK W. · 2011 to 2012
$84k
NCI NIH HHS P30 CA044579NIAAA NIH HHS AA10422NIAAA NIH HHS F31 AA019597NIAAA NIH HHS F31AA019597ANIAAA NIH HHS R01 AA010422NIAAA NIH HHS R37 AA010422
6 · The paper itself

Abstract

Ptp4a3 (commonly known as PRL-3) is an enigmatic member of the Ptp4a family of prenylated protein tyrosine phosphatases that are highly expressed in many human cancers. Despite strong correlations with tumor metastasis and poor patient prognosis, there is very limited understanding of this gene family's role in malignancy. Therefore, we created a gene-targeted murine knockout model for Ptp4a3, the most widely studied Ptp4a family member. Mice deficient for Ptp4a3 were grossly normal. Fewer homozygous-null males were observed at weaning, however, and they maintained a decreased body mass. Although Ptp4a3 is normally associated with late-stage cancer and metastasis, we observed increased Ptp4a3 expression in the colon of wildtype mice immediately following treatment with the carcinogen azoxymethane. To investigate the role of Ptp4a3 in malignancy, we used the most commonly studied murine colitis-associated colon cancer model. Wildtype mice treated with azoxymethane and dextran sodium sulfate developed approximately 7-10 tumors per mouse in the distal colon. The resulting tumor tissue had 4-fold more Ptp4a3 mRNA relative to normal colon epithelium and increased PTP4A3 protein. Ptp4a3-null mice developed 50% fewer colon tumors than wildtype mice after exposure to azoxymethane and dextran sodium sulfate. Tumors from the Ptp4a3-null mice had elevated levels of both IGF1Rβ and c-MYC compared to tumors replete with Ptp4a3, suggesting an enhanced cell signaling pathway engagement in the absence of the phosphatase. These results provide the first definitive evidence implicating Ptp4a3 in colon tumorigenesis and highlight the potential value of the phosphatase as a therapeutic target for early stage malignant disease.

Indexed as

AnimalsAzoxymethaneCarcinogensColonColonic NeoplasmsDextran SulfateGene DeletionHumansImmediate-Early ProteinsIntestinal MucosaMiceMice, KnockoutNeoplasm MetastasisNeoplasms, ExperimentalProtein Tyrosine PhosphatasesProto-Oncogene Proteins c-mycAzoxymethaneCarcinogensDextran SulfateImmediate-Early ProteinsMyc protein, mouseProtein Tyrosine PhosphatasesProto-Oncogene Proteins c-mycPtp4a3 protein, mouse

Identifiers

PMID23555575
PMCPMC3610886
OpenAlexW2078970119

What OpenQuestion holds

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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.