Evidence map›Paper›PMID 21466710›Full record

ArticleBMC cancer2011

Therapeutic potential of PRL-3 targeting and clinical significance of PRL-3 genomic amplification in gastric cancer.

Akira Ooki, Keishi Yamashita, Shiro Kikuchi, Shinichi Sakuramoto, Natsuya Katada, Mina Waraya, Hiroshi Kawamata, Hiroshi Nishimiya, Kazunori Nakamura, Masahiko Watanabe

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 25% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

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  10. 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
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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 2 institutions in 1 country.

Akira OokiDepartment of Surgery, Kitasato University Hospital, Kitasato 1-15-1, Sagamihara 228-8555, Kanagawa, Japan. sp9y9tq9@piano.ocn.ne.jp
Keishi Yamashita
Shiro Kikuchi
Shinichi Sakuramoto
Natsuya Katada
Mina Waraya
Hiroshi Kawamata
Hiroshi Nishimiya
Kazunori Nakamura
Masahiko Watanabe
Kitasato University · JPKitasato University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPhosphatase of regenerating liver-3 (PRL-3) has deserved attention as a crucial molecule in the multiple steps of metastasis. In the present study, we examined the mechanisms regulating PRL-3 expression, and assessed the clinical potential of PRL-3-targeted therapy in gastric cancer.

methodsPRL-3 genomic amplification was analyzed using quantitative-polymerase chain reaction and/or fluorescence in situ hybridization in 77 primary gastric tumors. The anticancer activity of PRL-3 inhibitor (1-4-bromo-2-benzylidene rhodanine) treatment was evaluated against cancer cells with different genetic and expression status.

resultsPRL-3 genomic amplification was closely concordant with high level of its protein expression in cell lines, and was found in 20% (8/40) among human primary tumors with its expression, which were all stage III/IV disease (40%, 8/20), but in none (0/37) among those without expression. Additionally, PRL-3 genomic amplification was associated with metastatic lymph node status, leading to advanced stage and thereby poor outcomes in patients with lymph node metastasis (P = 0.021). PRL-3 small interfering RNA robustly repressed metastatic properties, including cell proliferation, invasion, and anchorage-independent colony formation. Although neither PRL-3 genomic amplification nor expression level was responsible for the sensitivity to PRL-3 inhibitor treatment, the inhibitor showed dose-dependent anticancer efficacy, and remarkably induced apoptosis on all the tested cell lines with PRL-3 expression.

conclusionsWe have for the first time, demonstrated that PRL-3 genomic amplification is one of the predominant mechanisms inducing its expression, especially in more advanced stage, and that PRL-3-targeted therapy may have a great potential against gastric cancer with its expression.

Indexed as

ApoptosisBenzylidene CompoundsCell Growth ProcessesCell Line, TumorDisease ProgressionFemaleGene AmplificationGene Expression Regulation, NeoplasticHumansMaleNeoplasm InvasivenessNeoplasm MetastasisNeoplasm ProteinsNeoplasm StagingProtein Tyrosine PhosphatasesRhodanineBenzylidene CompoundsNeoplasm ProteinsProtein Tyrosine PhosphatasesPTP4A3 protein, humanRhodanineRNA, Small Interfering

Identifiers

PMID21466710
PMCPMC3080833
OpenAlexW1981589096

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.