Evidence map›Paper›PMID 27793041›Full record

ArticleOncotarget2016

CPI-17 drives oncogenic Ras signaling in human melanomas via Ezrin-Radixin-Moesin family proteins.

Lars Björn Riecken, Ansgar Zoch, Ulrike Wiehl, Sabine Reichert, Ingmar Scholl, Yan Cui, Mirjana Ziemer, Ulf Anderegg, Christian Hagel, Helen Morrison

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 43 citations in OpenAlex.

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  14. Review
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  16. Ezrin Mediates Invasion and Metastasis in Tumorigenesis: A Review.Frontiers in cell and developmental biology · 2020
    Review
  17. Article
  18. Article
  19. Detecting the location and significance of Ezrin protein expression in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2018
    Article
  20. 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

10 authors at 4 institutions in 2 countries.

Lars Björn RieckenLeibniz Institute on Aging, Fritz Lipmann Institute, Jena, Germany.
Ansgar ZochLeibniz Institute on Aging, Fritz Lipmann Institute, Jena, Germany.
Ulrike WiehlLeibniz Institute on Aging, Fritz Lipmann Institute, Jena, Germany.
Sabine ReichertLeibniz Institute on Aging, Fritz Lipmann Institute, Jena, Germany.
Ingmar SchollLeibniz Institute on Aging, Fritz Lipmann Institute, Jena, Germany.
Yan CuiLeibniz Institute on Aging, Fritz Lipmann Institute, Jena, Germany.
Mirjana ZiemerKlinik und Poliklinik für Dermatologie, Venerologie und Allergologie, Universität Leipzig, Leipzig, Germany.
Ulf AndereggKlinik und Poliklinik für Dermatologie, Venerologie und Allergologie, Universität Leipzig, Leipzig, Germany.
Christian HagelDepartment of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Helen MorrisonLeibniz Institute on Aging, Fritz Lipmann Institute, Jena, Germany.
Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DELeipzig University · DEUniversity College London · GBUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperactive Ras signaling has strong oncogenic effects causing several different forms of cancer. Hyperactivity is frequently induced by mutations within Ras itself, which account for up to 30% of all human cancers. In addition, hyperactive Ras signaling can also be triggered independent of Ras by either mutation or by misexpression of various upstream regulators and immediate downstream effectors. We have previously reported that C-kinase potentiated protein phosphatase-1 inhibitor of 17 kDa (CPI-17) can drive Ras activity and promote tumorigenic transformation by inhibition of the tumor suppressor Merlin. We now describe an additional element of this oncogenic mechanism in the form of the ezrin-radixin-moesin (ERM) protein family, which exhibits opposing roles in Ras activity control. Thus, CPI-17 drives Ras activity and tumorigenesis in a two-fold way; inactivation of the tumor suppressor merlin and activation of the growth promoting ERM family. The in vivo significance of this oncogenic switch is highlighted by demonstrating CPI-17's involvement in human melanoma pathogenesis.

Indexed as

AnimalsCell ProliferationCell Transformation, NeoplasticCytoskeletal ProteinsEzrinGene Expression Regulation, NeoplasticHeLa CellsHumansIntracellular Signaling Peptides and ProteinsMelanomaMembrane ProteinsMiceMicrofilament ProteinsMuscle ProteinsMyosin-Light-Chain PhosphataseNeurofibromin 2Cytoskeletal ProteinsEzrinIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicrofilament ProteinsmoesinMuscle ProteinsMyosin-Light-Chain PhosphataseNeurofibromin 2Phosphoprotein PhosphatasesPPP1R12A protein, humanPPP1R14A protein, humanradixinras ProteinscancerCPI-17ERMmelanomaRas

Identifiers

PMID27793041
PMCPMC5346635
OpenAlexW2541278309

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.