Evidence map›Paper›PMID 26975394›Full record

ArticleJournal of translational medicine2016

Phosphatase of regenerating liver 3 (PRL-3) is overexpressed in human prostate cancer tissue and promotes growth and migration.

Esten N Vandsemb, Helena Bertilsson, Pegah Abdollahi, Øystein Størkersen, Thea Kristin Våtsveen, Morten Beck Rye, Torstein Baade Rø, Magne Børset, Tobias S Slørdahl

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

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  10. Phosphatase of regenerating liver-3 regulates cancer cell metabolism in multiple myeloma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
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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

9 authors at 2 institutions in 1 country.

Esten N VandsembK. G. Jebsen Center for Myeloma Research, Norwegian University of Science and Technology, PO Box 8905, 7491, Trondheim, Norway. estennv@stud.ntnu.no.
Helena BertilssonDepartment of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Pegah AbdollahiK. G. Jebsen Center for Myeloma Research, Norwegian University of Science and Technology, PO Box 8905, 7491, Trondheim, Norway.
Øystein StørkersenDepartment of Pathology, Trondheim University Hospital, Trondheim, Norway.
Thea Kristin VåtsveenK. G. Jebsen Center for Myeloma Research, Norwegian University of Science and Technology, PO Box 8905, 7491, Trondheim, Norway.
Morten Beck RyeDepartment of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Torstein Baade RøK. G. Jebsen Center for Myeloma Research, Norwegian University of Science and Technology, PO Box 8905, 7491, Trondheim, Norway.
Magne BørsetK. G. Jebsen Center for Myeloma Research, Norwegian University of Science and Technology, PO Box 8905, 7491, Trondheim, Norway.
Tobias S SlørdahlK. G. Jebsen Center for Myeloma Research, Norwegian University of Science and Technology, PO Box 8905, 7491, Trondheim, Norway.
Norwegian University of Science and Technology · NOSt Olav's University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPRL-3 is a phosphatase implicated in oncogenesis in multiple cancers. In some cancers, notably carcinomas, PRL-3 is also associated with inferior prognosis and increased metastatic potential. In this study we investigated the expression of PRL-3 mRNA in fresh-frozen samples from patients undergoing radical prostatectomy because of prostate cancer (PC) and the biological function of PRL-3 in prostate cancer cells.

methodsSamples from 41 radical prostatectomy specimens (168 samples in total) divided into low (Gleason score ≤ 6), intermediate (Gleason score = 7) and high (Gleason score ≥ 8) risk were analyzed with gene expression profiling and compared to normal prostate tissue. PRL-3 was identified as a gene with differential expression between healthy and cancerous tissue in these analyses. We used the prostate cancer cell lines PC3 and DU145 and a small molecular inhibitor of PRL-3 to investigate whether PRL-3 had a functional role in cancer. Relative ATP-measurement and thymidine incorporation were used to assess the effect of PRL-3 on growth of the cancer cells. We performed an in vitro scratch assay to investigate the involvement of PRL-3 in migration. Immunohistochemistry was used to identify PRL-3 protein in prostate cancer primary tumor and corresponding lymph node metastases.

resultsCompared to normal prostate tissue, the prostate cancer tissue expressed a significantly higher level of PRL-3. We found PRL-3 to be present in both PC3 and DU145, and that inhibition of PRL-3 led to growth arrest and apoptosis in these two cell lines. Inhibition of PRL-3 led to reduced migration of the PC3 cells. Immunohistochemistry showed PRL-3 expression in both primary tumor and corresponding lymph node metastases.

conclusionsPRL-3 mRNA was expressed to a greater extent in prostate cancer tissue compared to normal prostate tissue. PRL-3 protein was expressed in both prostate cancer primary tumor and corresponding lymph node metastases. The results from our in vitro assays suggest that PRL-3 promotes growth and migration in prostate cancer. In conclusion, these results imply that PRL-3 has a role in the pathogenesis of prostate cancer.

Indexed as

Cell MovementCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalGenetic LociHumansLymphatic MetastasisMaleNeoplasm ProteinsProstatic NeoplasmsProtein Tyrosine PhosphatasesTissue Array AnalysisNeoplasm ProteinsProtein Tyrosine PhosphatasesPTP4A3 protein, humanMolecular pathogenesisOncogenesisPRL-3Prostate cancerPTP4A3

Identifiers

PMID26975394
PMCPMC4791872
OpenAlexW2300882941

What OpenQuestion holds

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LicenceCC BY
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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.