Evidence map›Paper›PMID 27176481›Full record

ArticleJournal of experimental & clinical cancer research : CR2016

PI3K p110β isoform synergizes with JNK in the regulation of glioblastoma cell proliferation and migration through Akt and FAK inhibition.

Hua-Fu Zhao, Jing Wang, Hao-Ran Jiang, Zhong-Ping Chen, Shing-Shun Tony To

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
2.3field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 42 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Formyl Peptide Receptor-2-Suppressed Autophagy Promotes the Migration and Invasion of Human Glioblastoma Cells Through PI3K/Akt Signaling.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
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  12. Targeting RTK-PI3K-mTOR Axis in Gliomas: An Update.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Selective inhibitors for JNK signalling: a potential targeted therapy in cancer.Journal of enzyme inhibition and medicinal chemistry · 2020
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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

5 authors at 5 institutions in 2 countries.

Hua-Fu ZhaoDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong, China.
Jing WangDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong, China.
Hao-Ran JiangDepartment of Neurosurgery, Huizhou First People's Hospital, Huizhou, 516003, China.
Zhong-Ping ChenDepartment of Neurosurgery/Neuro-oncology, Sun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, 510060, China. chenzhp@sysucc.org.cn.
Shing-Shun Tony ToDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong, China. tony.to@polyu.edu.hk.
Hong Kong Polytechnic University · HKHuizhou Central People's Hospital · CNShenzhen Second People's Hospital · CNSun Yat-sen University · CNSun Yat-sen University Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlioblastoma multiforme is the most aggressive malignant primary brain tumor, characterized by rapid growth and extensive infiltration to neighboring normal brain parenchyma. Both PI3K/Akt and JNK pathways are essential to glioblastoma cell survival, migration and invasion. Due to their hyperactivation in glioblastoma cells, PI3K and JNK are promising targets for glioblastoma treatment.

methodsTo investigate the combination effects of class IA PI3K catalytic isoforms (p110α, p110β and p110δ) and JNK inhibition on tumor cell growth and motility, glioblastoma cells and xenografts in nude mice were treated with isoform-selective PI3K inhibitors in combination with JNK inhibitor.

resultsWe showed that combined inhibition of these PI3K isoforms and JNK exerted divergent effects on the proliferation, migration and invasion of glioblastoma cells in vitro. Pharmacological inhibition of p110β or p110δ, but not p110α, displayed synergistic inhibitory effect with JNK inhibition on glioblastoma cell proliferation and migration through decreasing phosphorylation of Akt, FAK and zyxin, leading to blockade of lamellipodia and membrane ruffles formation. No synergistic effect on invasion was observed in all the combination treatment. In vivo, combination of p110β and JNK inhibitors significantly reduced xenograft tumor growth compared with single inhibitor alone.

conclusionConcurrent inhibition of p110β and JNK exhibited synergistic effects on suppressing glioblastoma cell proliferation and migration in vitro and xenograft tumor growth in vivo. Our data suggest that combined inhibition of PI3K p110β isoform and JNK may serve as a potent and promising therapeutic approach for glioblastoma multiforme.

Indexed as

AnimalsBrain NeoplasmsCell Line, TumorCell MovementCell ProliferationCell SurvivalFocal Adhesion Kinase 1Gene Expression Regulation, NeoplasticGlioblastomaHumansMAP Kinase Kinase 4MiceNeoplasm TransplantationPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationFocal Adhesion Kinase 1MAP Kinase Kinase 4Phosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPTK2 protein, humanGlioblastomaJNKMigrationp110βPI3KProliferationSynergism

Identifiers

PMID27176481
PMCPMC4866398
OpenAlexW2367511620

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.