Evidence map›Paper›PMID 32126150›Full record

ArticleJournal of cellular and molecular medicine2020

Inhibition of PLK4 might enhance the anti-tumour effect of bortezomib on glioblastoma via PTEN/PI3K/AKT/mTOR signalling pathway.

Jing Wang, Dengpeng Ren, Yan Sun, Chao Xu, Chunhong Wang, Rui Cheng, Lina Wang, Guijun Jia, Jinrui Ren, Jiuhong Ma and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

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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

12 authors at 4 institutions in 1 country.

Jing WangDepartment of neurosurgery, Shanxi academy of medical science, Shanxi Bethune Hospital, Taiyuan, China.ORCID 0000-0002-4394-7689
Dengpeng RenDepartment of neurosurgery, Central Hospital of Yuncheng city, Yuncheng, China.
Yan SunNeurological intensive care unit, Special medical center of PAP, Tianjin, China.
Chao XuNeurological intensive care unit, Special medical center of PAP, Tianjin, China.
Chunhong WangDepartment of neurosurgery, Shanxi people's hospital, Taiyuan, China.
Rui ChengDepartment of neurosurgery, Shanxi people's hospital, Taiyuan, China.
Lina WangNeurological intensive care unit, Special medical center of PAP, Tianjin, China.
Guijun JiaDepartment of neurosurgery, Shanxi people's hospital, Taiyuan, China.
Jinrui RenDepartment of neurosurgery, Shanxi people's hospital, Taiyuan, China.
Jiuhong MaDepartment of neurosurgery, Shanxi people's hospital, Taiyuan, China.
Yue TuNeurological intensive care unit, Special medical center of PAP, Tianjin, China.
Hongming JiDepartment of neurosurgery, Shanxi people's hospital, Taiyuan, China.
Shanxi Province Hospital of Traditional Chinese Medicine · CNTianjin Medical University · CNShanxi Academy of Medical Sciences · CNYuncheng University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is one of the most common aggressive cancers of the central nervous system in adults with a high mortality rate. Bortezomib is a boronic acid-based potent proteasome inhibitor that has been actively studied for its anti-tumour effects through inhibition of the proteasome. The proteasome is a key component of the ubiquitin-proteasome pathway that is critical for protein homeostasis, regulation of cellular growth, and apoptosis. Overexpression of polo-like kinase 4 (PLK4) is commonly reported in tumour cells and increases their invasive and metastatic abilities. In this study, we established a cell model of PLK4 knockdown and overexpression in LN-18, A172 and LN-229 cells and found that knockdown of PLK4 expression enhanced the anti-tumour effect of bortezomib. We further found that this effect may be mediated by the PTEN/PI3K/AKT/mTOR signalling pathway and that the apoptotic and oxidative stress processes were activated, while the expression of matrix metalloproteinases (MMPs) was down-regulated. Similar phenomenon was observed using in vitro experiments. Thus, we speculate that PLK4 inhibition may be a new therapeutic strategy for GBM.

Indexed as

AnimalsApoptosisBoronic AcidsBortezomibCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGlioblastomaHeterograftsHumansMicePhosphatidylinositol 3-KinasesProteasome InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseBoronic AcidsBortezomibPhosphatidylinositol 3-KinasesPLK4 protein, humanProteasome InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTOR Serine-Threonine KinasesbortezomibglioblastomaPLK4PTEN/PI3K/AKT/mTOR signalling pathway

Identifiers

PMID32126150
PMCPMC7171416
OpenAlexW3009836641

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.