Evidence map›Paper›PMID 30531692›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2018

High Mobility Group Box 1 (HMGB1) Predicts Invasion and Poor Prognosis of Glioblastoma Multiforme via Activating AKT Signaling in an Autocrine Pathway.

Peng Cheng, Yun Ma, Zhiqiang Gao, Lingling Duan

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 32 citations in OpenAlex.

  1. Tumor-intrinsic TLR4 signaling as a context-dependent rheostat in glioblastoma.Journal of molecular medicine (Berlin, Germany) · 2026
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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

4 authors at 2 institutions in 1 country.

Peng ChengDepartment of Critical Care Medicine, Yidu Central Hospital of Weifang, Weifang, Shandong, China (mainland).
Yun MaDepartment of Critical Care Medicine, Yidu Central Hospital of Weifang, Weifang, Shandong, China (mainland).
Zhiqiang GaoDepartment of Nephrology, Yidu Central Hospital of Weifang, Weifang, Shandong, China (mainland).
Lingling DuanDepartment of Geriatric Medicine, Jinan Central Hospital of Shandong University, Jinan, Shandong, China (mainland).
Yidu Central Hospital of Weifang · CNJinan Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND As a nuclear protein and a secreted protein, HMGB1 is involved in many cellular processes such as proliferation, transcription, and inflammation. The overexpression of HMGB1 in various types of cancers is reported, but its clinical significance and prognostic value in glioblastoma multiforme (GBM) has not been well defined. MATERIAL AND METHODS The expression of HMGB1 in 116 patients with GBM was investigated with immunohistochemistry, and was detected with qRT-PCR in 12 pairs of tumor tissues and adjacent tissues. The correlations between HMGB1 and clinicopathological factors were analyzed with the chi-square test. Prognostic value of HMGB1 was evaluated with univariate analysis and multivariate analysis. By knocking down HMGB1 by siRNA, the functions of HMGB1 in progression of GBM cell lines were investigated by experiments in vitro. RESULTS In our study, patients with high HMGB1 expression accounted for 42.2% of all the patients. High HMGB1 was correlated with low survival rates and was identified as an independent prognostic factor of GBM. Knockdown of intracellular HMGB1 remarkably decreased GBM cells proliferation and invasion. In hypoxia, intracellular HMGB1 of GBM cells was released out and activated AKT and ERK signaling pathways, thus promoting GBM cell invasion in this autocrine pathway. CONCLUSIONS HMGB1 is an independent prognostic biomarker for unfavorable prognosis of patients with GBM. Released HMGB1 of GBM cells can activate AKT and ERK signaling pathways and promote GBM cells invasion in this autocrine pathway, indicating that anti-HMGB1 therapy may be a promising treatment for GBM.

Indexed as

AdultAutocrine CommunicationBrain NeoplasmsCell Line, TumorCell ProliferationDisease ProgressionFemaleGlioblastomaHMGB1 ProteinHumansImmunohistochemistryKaplan-Meier EstimateMaleMiddle AgedNeoplasm InvasivenessPrognosisHMGB1 ProteinHMGB1 protein, humanProto-Oncogene Proteins c-akt

Identifiers

PMID30531692
PMCPMC6296343
OpenAlexW2978401336

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.