Evidence map›Paper›PMID 29740218›Full record

ArticleCancer management and research2018

Paeoniflorin inhibits glioblastoma growth in vivo and in vitro: a role for the Triad3A-dependent ubiquitin proteasome pathway in TLR4 degradation.

Zhaotao Wang, Guoyong Yu, Zhi Liu, Jianwei Zhu, Chen Chen, Ru-En Liu, Ruxiang Xu

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

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  11. Intranasal delivery of paeoniflorin nanocrystals for brain targeting.Asian journal of pharmaceutical sciences · 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

7 authors at 4 institutions in 1 country.

Zhaotao Wang *Department of Neurosurgery, Affiliated Bayi Brain Hospital, General Army Hospital, Southern Medical University, Beijing, China.
Guoyong Yu *Department of Neurosurgery, Jiangxi Provincial People's Hospital, Nanchang, China.
Zhi LiuDepartment of Neurosurgery, Peking University People's Hospital, Peking University, Beijing, China.
Jianwei ZhuDepartment of Neurosurgery, Affiliated Hospital of Traditional Chinese Medicine, Southwest Medical University, Luzhou, China.
Chen ChenDepartment of Neurosurgery, Affiliated Bayi Brain Hospital, General Army Hospital, Southern Medical University, Beijing, China.
Ru-En LiuDepartment of Neurosurgery, Peking University People's Hospital, Peking University, Beijing, China.
Ruxiang XuDepartment of Neurosurgery, Affiliated Bayi Brain Hospital, General Army Hospital, Southern Medical University, Beijing, China.
Southern Medical University · CNPeking University · CNJiangxi Provincial People's Hospital · CNSouthwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPaeoniflorin, a polyphenolic compound derived from

methodsCCK-8 experiments and clone formation assay were performed to detect the cell proliferation. Western blotting was used to analyze protein expression levels. Detection of Triad3A binding with TLR4 was assessed by the immunoprecipitation. Orthotopic xenograft mouse model was used to evaluate the effect of paeoniflorin in vivo. MST was used to analyze the interaction between paeoniflorin and TLR4 protein.

resultsIn our study, we found that paeoniflorin effectively inhibited glioblastoma growth and suppressed TLR4 protein levels, as well its downstream effectors both in vivo and in vitro. Moreover, when overexpressed TLR4 in glioblastoma abolished the effects of paeoniflorin on cell proliferation, migration, and invasion. Furthermore, we found that paeoniflorin decreased TLR4 protein through ubiquitination proteasome pathway (UPP)-mediated degradation in glioblastoma cells. Mechanistically, paeoniflorin promoted Triad3A to conjugate with TLR4, resulting in degradation. In addition,

conclusionOur study is the first to identify a novel mechanism for the antitumor activity of paeoniflorin, specifically: it decreases tumor growth by directly targeting TLR4 and modulating the TLR4/Triad3A-dependent axis, leading to TLR4 protein degradation and inhibition of glioblastoma cell progression in vitro and in vivo. Our current findings indicate that paeoniflorin is a potential glioblastoma therapeutic agent due to its Triad3A-dependent ubiquitin degradation of TLR4.

Indexed as

glioblastomapaeoniflorinTLR4Triad3Aubiquitin

Identifiers

PMID29740218
PMCPMC5931203
OpenAlexW2801310433

What OpenQuestion holds

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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.