Evidence map›Paper›PMID 26700818›Full record

ArticleOncotarget2016

PKCδ activated by c-MET enhances infiltration of human glioblastoma cells through NOTCH2 signaling.

Eunji Hwang, Ki-Chun Yoo, Seok-Gu Kang, Rae-Kwon Kim, Yan-Hong Cui, Hae-June Lee, Min-Jung Kim, Jae-Seong Lee, In-Gyu Kim, Yongjoon Suh 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 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. MET in glioma: signaling pathways and targeted therapies.Journal of experimental & clinical cancer research : CR · 2019
    Review
  5. Review
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  7. Article
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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 5 institutions in 1 country.

Eunji HwangDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.
Ki-Chun YooDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.
Seok-Gu KangDepartment of Neurosurgery, Severance Hospital, Yonsei University College of Medicine, Seodaemun-gu, Korea.
Rae-Kwon KimDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.
Yan-Hong CuiDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.
Hae-June LeeDivision of Radiation Effect, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Min-Jung KimLaboratory of Radiation Exposure & Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Jae-Seong LeeDepartment of Biological Sciences, College of Science, Sungkyunkwan University, Seoul, Korea.
In-Gyu KimDepartment of Radiation Biology, Environmental Radiation Research Group, Korea Atomic Energy Research Institute, Daejeon, Korea.
Yongjoon SuhDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.
Su-Jae LeeDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.
Hanyang University · KRKorea Institute of Radiological and Medical Sciences · KRKorea Atomic Energy Research Institute · KRSungkyunkwan University · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Poor prognosis of glioblastoma (GBM) is attributable to the propensity of tumor cells to infiltrate into the brain parenchyma. Protein kinase C (PKC) isozymes are highly expressed or aberrantly activated in GBM. However, how this signaling node translates to GBM cell invasiveness remains unknown. Here, we report that among PKC isoforms, PKCδ is strongly associated with infiltration of GBM cells. Notably, PKCδ enhanced Tyr418 phosphorylation of the non-receptor tyrosine kinase SRC, which in turn activated STAT3 and subsequent NOTCH2 signaling, ultimately leading to GBM cell invasiveness. Furthermore, we showed that PKCδ was aberrantly activated in GBM cells by c-MET, a receptor tyrosine kinase hyperactivated in GBM. In agreement, inhibition either component in the c-MET/PKCδ/SRC/STAT3 signaling axis effectively blocked the NOTCH2 signaling and invasiveness of GBM cells. Taken together, our findings shed a light on the signaling mechanisms behind the constitutive activation of PKCδ signaling in GBM.

Indexed as

AgedAnimalsApoptosisBiomarkers, TumorBlotting, WesternCell MovementCell ProliferationFemaleGlioblastomaHumansImmunoenzyme TechniquesMiceMice, Inbred BALB CMice, NudeProtein Kinase C-deltaProto-Oncogene Proteins c-metBiomarkers, TumorNOTCH2 protein, humanProtein Kinase C-deltaProto-Oncogene Proteins c-metReceptor, Notch2RNA, Messengerc-METglioblastomainfiltrationNOTCH2PKCδ

Identifiers

PMID26700818
PMCPMC4826251
OpenAlexW2270493970

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.