Evidence map›Paper›PMID 31778016›Full record

ArticleJournal of cellular and molecular medicine2020

Reduced expression of proteolipid protein 2 increases ER stress-induced apoptosis and autophagy in glioblastoma.

Zichao Feng, Wenjing Zhou, Jiwei Wang, Qichao Qi, Mingzhi Han, Yang Kong, Yaotian Hu, Yulin Zhang, Anbin Chen, Bin Huang and 8 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 15 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

18 authors at 2 institutions in 3 countries.

Zichao FengDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.ORCID 0000-0001-7543-6122
Wenjing ZhouDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Jiwei WangDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Qichao QiDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Mingzhi HanDepartment of Biomedicine, University of Bergen, Bergen, Norway.
Yang KongDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Yaotian HuDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Yulin ZhangDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Anbin ChenDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Bin HuangDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Anjing ChenDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Di ZhangDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Wenjie LiDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Qing ZhangDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Rolf BjerkvigDepartment of Biomedicine, University of Bergen, Bergen, Norway.
Jian WangDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Frits ThorsenDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.ORCID 0000-0002-7762-3703
Xingang LiDepartment of Neurosurgery, Qilu Hospital of Shandong University, Shandong Key Laboratory of Brain Functional Remodeling and Brain Science Research Institute, Shandong University, Shandong, China.
Qilu Hospital of Shandong University · CNLuxembourg Institute of Health · LU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteolipid protein 2 (PLP2) is an integral ion channel membrane protein of the endoplasmic reticulum. The protein has been shown to be highly expressed in many cancer types, but its importance in glioma progression is poorly understood. Using publicly available datasets (Rembrandt, TCGA and CGGA), we found that the expression of PLP2 was significantly higher in high-grade gliomas than in low-grade gliomas. We confirmed these results at the protein level through IHC staining of high-grade (n = 56) and low-grade glioma biopsies (n = 16). Kaplan-Meier analysis demonstrated that increased PLP2 expression was associated with poorer patient survival. In functional experiments, siRNA and shRNA PLP2 knockdown induced ER stress and increased apoptosis and autophagy in U87 and U251 glioma cell lines. Inhibition of autophagy with chloroquine augmented apoptotic cell death in U87- and U251-siPLP2 cells. Finally, intracranial xenografts derived from U87- and U251-shPLP2 cells revealed that loss of PLP2 reduced glioma growth in vivo. Our results therefore indicate that increased PLP2 expression promotes GBM growth and that PLP2 represents a potential future therapeutic target.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisAutophagyBrain NeoplasmsCell Line, TumorCell ProliferationDown-RegulationEndoplasmic Reticulum StressGene Knockdown TechniquesGlioblastomaHumansMaleMARVEL Domain-Containing ProteinsMicePrognosisMARVEL Domain-Containing ProteinsPLP2 protein, humanProteolipidsTranscription Factor CHOPapoptosisautophagyER stressglioblastomaproteolipid protein 2

Identifiers

PMID31778016
PMCPMC7077595
OpenAlexW2989656366

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.