Evidence map›Paper›PMID 27626684›Full record

ArticleOncotarget2016

Exclusive inhibition of PI3K/Akt/mTOR signaling is not sufficient to prevent PDGF-mediated effects on glycolysis and proliferation in colorectal cancer.

Romana Moench, Tanja Grimmig, Vinicius Kannen, Sudipta Tripathi, Marc Faber, Eva-Maria Moll, Anil Chandraker, Reinhard Lissner, Christoph-Thomas Germer, Ana Maria Waaga-Gasser and 1 more

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 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

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  8. The Genomic Environment ofJournal of clinical medicine · 2022
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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

11 authors at 4 institutions in 3 countries.

Romana MoenchDepartment of Surgery I, Molecular Oncology and Immunology, University of Wuerzburg, Wuerzburg, Germany.
Tanja GrimmigDepartment of Surgery I, Molecular Oncology and Immunology, University of Wuerzburg, Wuerzburg, Germany.
Vinicius KannenRibeirao Preto Pharmaceutical Sciences School, Department of Toxicology, Bromatology, and Clinical Analysis, University of Sao Paulo, Sao Paulo, Brazil.
Sudipta TripathiBrigham and Women's Hospital, Transplant Research Center, Harvard Medical School, Boston, MA, USA.
Marc FaberDepartment of Surgery I, Molecular Oncology and Immunology, University of Wuerzburg, Wuerzburg, Germany.
Eva-Maria MollDepartment of Surgery I, Molecular Oncology and Immunology, University of Wuerzburg, Wuerzburg, Germany.
Anil ChandrakerBrigham and Women's Hospital, Transplant Research Center, Harvard Medical School, Boston, MA, USA.
Reinhard LissnerDepartment of Surgery I, Molecular Oncology and Immunology, University of Wuerzburg, Wuerzburg, Germany.
Christoph-Thomas GermerDepartment of Surgery I, University of Wuerzburg, Wuerzburg, Germany.
Ana Maria Waaga-GasserDepartment of Surgery I, Molecular Oncology and Immunology, University of Wuerzburg, Wuerzburg, Germany.
Martin GasserDepartment of Surgery I, University of Wuerzburg, Wuerzburg, Germany.
University of Würzburg · DEHarvard University · USBrigham and Women's Hospital · USUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Platelet-derived growth factor (PDGF) and signaling via its receptors plays a crucial role in tumor cell proliferation and thus may represent an attractive target besides VEGF/EGFR-based antibody therapies. In this study we analyzed the influence of PDGF in colorectal cancer. PDGF was expressed intensively in early and even more intensively in late stage primary CRCs. Like VEGF, PDGF enhanced human colon cancer proliferation, and increased oxidative glycolytic activity, and activated HIF1α and c-Myc in vitro. PDGF activated the PI3K/Akt/mTOR pathway while leaving MAPK signaling untouched. Further dissection showed that inhibition of Akt strongly impeded cancer cell growth while inhibition of PI3K did not. MAPK analysis suggested an inhibitory crosstalk between both pathways, thus explaining the different effects of the Akt and PI3K inhibitors on cancer cell proliferation. PDGF stimulates colon cancer cell proliferation, and prevents inhibitor induced apoptosis, resulting in tumor growth. Therefore inhibition of PDGF signaling seems to be a promising target in colorectal cancer therapy. However, due to the multifaceted nature of the intracellular PDGF signaling, careful intervention strategies are needed when looking into specific signaling pathways like PI3K/Akt/mTOR and MAPK.

Indexed as

ApoptosisCell Line, TumorCell ProliferationColorectal NeoplasmsGlycolysisHCT116 CellsHT29 CellsHumansMAP Kinase Signaling SystemPhosphatidylinositol 3-KinasesPlatelet-Derived Growth FactorProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesVascular Endothelial Growth Factor AMTOR protein, humanPhosphatidylinositol 3-KinasesPlatelet-Derived Growth FactorProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesVascular Endothelial Growth Factor Acolorectal cancerglucose metabolismMAPK pathwayPDGFPI3K/Akt/mTOR

Identifiers

PMID27626684
PMCPMC5356587
OpenAlexW2517068759

What OpenQuestion holds

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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.