Evidence map›Paper›PMID 26254477›Full record

ArticleNeuro-oncology2016

Loss of endothelial programmed cell death 10 activates glioblastoma cells and promotes tumor growth.

Yuan Zhu, Kai Zhao, Anja Prinz, Kathy Keyvani, Nicole Lambertz, Ilonka Kreitschmann-Andermahr, Ting Lei, Ulrich Sure

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 20% 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, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  15. The multifacetedGenes & diseases · 2021
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  20. Novel exosomal miR-46146 transfer oxaliplatin chemoresistance in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    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

8 authors at 2 institutions in 2 countries.

Yuan ZhuDepartment of Neurosurgery, University of Duisburg-Essen, Essen, Germany (Y.Z., K.Z., A.P., N.L., I.K.-A., U.S.); Institute of Neuropathology, University of Duisburg-Essen, Essen, Germany (K.K.); Department of Neurosurgery, Tongji Medical College, Wuhan, China (K.Z., T.L.).
Kai ZhaoDepartment of Neurosurgery, University of Duisburg-Essen, Essen, Germany (Y.Z., K.Z., A.P., N.L., I.K.-A., U.S.); Institute of Neuropathology, University of Duisburg-Essen, Essen, Germany (K.K.); Department of Neurosurgery, Tongji Medical College, Wuhan, China (K.Z., T.L.).
Anja PrinzDepartment of Neurosurgery, University of Duisburg-Essen, Essen, Germany (Y.Z., K.Z., A.P., N.L., I.K.-A., U.S.); Institute of Neuropathology, University of Duisburg-Essen, Essen, Germany (K.K.); Department of Neurosurgery, Tongji Medical College, Wuhan, China (K.Z., T.L.).
Kathy KeyvaniDepartment of Neurosurgery, University of Duisburg-Essen, Essen, Germany (Y.Z., K.Z., A.P., N.L., I.K.-A., U.S.); Institute of Neuropathology, University of Duisburg-Essen, Essen, Germany (K.K.); Department of Neurosurgery, Tongji Medical College, Wuhan, China (K.Z., T.L.).
Nicole LambertzDepartment of Neurosurgery, University of Duisburg-Essen, Essen, Germany (Y.Z., K.Z., A.P., N.L., I.K.-A., U.S.); Institute of Neuropathology, University of Duisburg-Essen, Essen, Germany (K.K.); Department of Neurosurgery, Tongji Medical College, Wuhan, China (K.Z., T.L.).
Ilonka Kreitschmann-AndermahrDepartment of Neurosurgery, University of Duisburg-Essen, Essen, Germany (Y.Z., K.Z., A.P., N.L., I.K.-A., U.S.); Institute of Neuropathology, University of Duisburg-Essen, Essen, Germany (K.K.); Department of Neurosurgery, Tongji Medical College, Wuhan, China (K.Z., T.L.).
Ting LeiDepartment of Neurosurgery, University of Duisburg-Essen, Essen, Germany (Y.Z., K.Z., A.P., N.L., I.K.-A., U.S.); Institute of Neuropathology, University of Duisburg-Essen, Essen, Germany (K.K.); Department of Neurosurgery, Tongji Medical College, Wuhan, China (K.Z., T.L.).
Ulrich SureDepartment of Neurosurgery, University of Duisburg-Essen, Essen, Germany (Y.Z., K.Z., A.P., N.L., I.K.-A., U.S.); Institute of Neuropathology, University of Duisburg-Essen, Essen, Germany (K.K.); Department of Neurosurgery, Tongji Medical College, Wuhan, China (K.Z., T.L.).
Tongji Hospital · CNUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeo-angiogenesis is a hallmark of glioblastoma (GBM) and is sustained by autocrine and paracrine interactions between neoplastic and nonneoplastic cells. Programmed cell death 10 (PDCD10) is ubiquitously expressed in nearly all tissues and plays crucial roles in regulating angiogenesis and apoptosis. We recently discovered the absence of PDCD10 expression in the tumor vessels of GBM patients. This raised the hypothesis that loss of endothelial PDCD10 affected GBM cell phenotyping and tumor progression.

methodsEndothelial PDCD10 was silenced by siRNA and lentiviral shRNA. The tumor cell phenotype was studied in direct and indirect co-culture of endothelial cells (ECs) with U87 or LN229. Angiogenic protein array was performed in the media of PDCD10-silenced ECs. Tumor angiogenesis and tumor growth were investigated in a human GBM xenograft mouse model.

resultsEndothelial silence of PDCD10 significantly stimulated tumor cell proliferation, migration, adhesion, and invasion and inhibited apoptosis in co-cultures. Stable knockdown of endothelial PDCD10 increased microvessel density and the formation of a functional vascular network, leading to a 4-fold larger tumor mass in mice. Intriguingly, endothelial deletion of PDCD10 increased (≥2-fold) the release of 20 of 55 tested proangiogenic factors including VEGF, which in turn activated Erk1/2 and Akt in GBM cells.

conclusionsFor the first time, we provide evidence that loss of endothelial PDCD10 activates GBM cells and promotes tumor growth, most likely via a paracrine mechanism. PDCD10 shows a tumor-suppressor-like function in the cross talk between ECs and tumor cells and is potentially implicated in GBM progression.

Indexed as

Cell MovementCell ProliferationAnimalsApoptosisApoptosis Regulatory ProteinsBlotting, WesternBrain NeoplasmsCoculture TechniquesFemaleFluorescent Antibody TechniqueGene Expression Regulation, NeoplasticGlioblastomaHumansHuman Umbilical Vein Endothelial CellsImmunoenzyme TechniquesMembrane ProteinsApoptosis Regulatory ProteinsMembrane ProteinsPDCD10 protein, humanProto-Oncogene ProteinsRNA, Small Interferingangiogenesisendothelial cellsglioblastomaPDCD10/CCM3

Identifiers

PMID26254477
PMCPMC4799675
OpenAlexW2300389549

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.