Evidence map›Paper›PMID 21750652›Full record

ArticleNeoplasia (New York, N.Y.)2011

Matrix-dependent regulation of AKT in Hepsin-overexpressing PC3 prostate cancer cells.

Stephanie M Wittig-Blaich, Lukasz A Kacprzyk, Thorsten Eismann, Melanie Bewerunge-Hudler, Petra Kruse, Eva Winkler, Wolfgang S L Strauss, Raimund Hibst, Rudolf Steiner, Mark Schrader and 3 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

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  18. The interconnectedness of cancer cell signaling.Neoplasia (New York, N.Y.) · 2011
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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

13 authors at 1 institution in 1 country.

Stephanie M Wittig-BlaichGerman Cancer Research Centre and National Center for Tumour Diseases, Cancer Genome Research Unit, Heidelberg, Germany.
Lukasz A Kacprzyk
Thorsten Eismann
Melanie Bewerunge-Hudler
Petra Kruse
Eva Winkler
Wolfgang S L Strauss
Raimund Hibst
Rudolf Steiner
Mark Schrader
Daniel Mertens
Holger Sültmann
Rainer Wittig
Universität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The serine-protease hepsin is one of the most prominently overexpressed genes in human prostate carcinoma. Forced expression of the enzyme in mice prostates is associated with matrix degradation, invasive growth, and prostate cancer progression. Conversely, hepsin overexpression in metastatic prostate cancer cell lines was reported to induce cell cycle arrest and reduction of invasive growth in vitro. We used a system for doxycycline (dox)-inducible target gene expression in metastasis-derived PC3 cells to analyze the effects of hepsin in a quantitative manner. Loss of viability and adhesion correlated with hepsin expression levels during anchorage-dependent but not anchorage-independent growth. Full expression of hepsin led to cell death and detachment and was specifically associated with reduced phosphorylation of AKT at Ser(473), which was restored by growth on matrix derived from RWPE1 normal prostatic epithelial cells. In the chorioallantoic membrane xenograft model, hepsin overexpression in PC3 cells reduced the viability of tumors but did not suppress invasive growth. The data presented here provide evidence that elevated levels of hepsin interfere with cell adhesion and viability in the background of prostate cancer as well as other tissue types, the details of which depend on the microenvironment provided. Our findings suggest that overexpression of the enzyme in prostate carcinogenesis must be spatially and temporally restricted for the efficient development of tumors and metastases.

Indexed as

AdenocarcinomaAnimalsCell Line, TumorChick EmbryoExtracellular MatrixGene Expression Regulation, NeoplasticHumansMaleMiceNeoplasm InvasivenessProstatic NeoplasmsProto-Oncogene Proteins c-aktSerine EndopeptidasesTransfectionTransplantation, HeterologousUp-RegulationhepsinProto-Oncogene Proteins c-aktSerine Endopeptidases

Identifiers

PMID21750652
PMCPMC3132844
OpenAlexW1528543854

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.