Evidence map›Paper›PMID 30542512›Full record

ArticleOncotarget2018

Diverse effects of phospholipase A2 receptor expression on LNCaP and PC-3 prostate cancer cell growth

Markus Friedemann, Brit Nacke, Albert Hagelgans, Carsten Jandeck, Nicole Bechmann, Martin Ullrich, Birgit Belter, Christin Neuber, Olga Sukocheva, Jens Pietzsch and 1 more

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

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

6 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  3. Review
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  6. Review
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

11 authors at 4 institutions in 2 countries.

Markus FriedemannTechnische Universität Dresden, Carl Gustav Carus University Hospital Dresden, Institute of Clinical Chemistry and Laboratory Medicine, 01307 Dresden, Germany.
Brit NackeTechnische Universität Dresden, Carl Gustav Carus University Hospital Dresden, Institute of Clinical Chemistry and Laboratory Medicine, 01307 Dresden, Germany.
Albert HagelgansTechnische Universität Dresden, Carl Gustav Carus University Hospital Dresden, Institute of Clinical Chemistry and Laboratory Medicine, 01307 Dresden, Germany.
Carsten JandeckTechnische Universität Dresden, Carl Gustav Carus University Hospital Dresden, Institute of Clinical Chemistry and Laboratory Medicine, 01307 Dresden, Germany.
Nicole BechmannTechnische Universität Dresden, Carl Gustav Carus University Hospital Dresden, Institute of Clinical Chemistry and Laboratory Medicine, 01307 Dresden, Germany.
Martin UllrichHelmholtz-Zentrum Dresden-Rossendorf, Institute of Radiopharmaceutical Cancer Research, Department of Radiopharmaceutical and Chemical Biology, 01328 Dresden, Germany.
Birgit BelterHelmholtz-Zentrum Dresden-Rossendorf, Institute of Radiopharmaceutical Cancer Research, Department of Radiopharmaceutical and Chemical Biology, 01328 Dresden, Germany.
Christin NeuberHelmholtz-Zentrum Dresden-Rossendorf, Institute of Radiopharmaceutical Cancer Research, Department of Radiopharmaceutical and Chemical Biology, 01328 Dresden, Germany.
Olga SukochevaSchool of Health Sciences, Flinders University of South Australia, Bedford Park 5042, Australia.
Jens PietzschHelmholtz-Zentrum Dresden-Rossendorf, Institute of Radiopharmaceutical Cancer Research, Department of Radiopharmaceutical and Chemical Biology, 01328 Dresden, Germany.
Mario MenschikowskiTechnische Universität Dresden, Carl Gustav Carus University Hospital Dresden, Institute of Clinical Chemistry and Laboratory Medicine, 01307 Dresden, Germany.
TU Dresden · DEHelmholtz-Zentrum Dresden-Rossendorf · DEUniversity Hospital Carl Gustav Carus · DEFlinders University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Physiological and pathophysiological functions of the phospholipase A2 receptor 1 (PLA2R1) are still not completely understood. To elucidate PLA2R1's function in prostate carcinoma, the receptor was ectopically overexpressed in LNCaP with silenced PLA2R1, and diminished in PC-3 cells with constitutively increased PLA2R1 expression relative to normal prostate epithelial cells. LNCaP cells were transfected to overexpress PLA2R1 (LNCaP-PLA2R1) and compared to control vector transfected cells (LNCaP-Ctrl). Alternatively, a CRISPR/Cas9-knockdown of PLA2R1 was achieved in PC-3 cells (PC-3 KD) and compared to the corresponding control-transfected cells (PC-3 Ctrl). The impact of PLA2R1 expression on proliferative and metastatic parameters was analysed

Indexed as

colony formationLNCaP and PC-3 prostate cancer cellsPLA2R1 transfectionproliferationxenograft mouse model

Identifiers

PMID30542512
PMCPMC6267604
OpenAlexW2901113762

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.