Evidence map›Paper›PMID 29423667›Full record

ArticleNeurochemical research2018

Paeoniflorin Inhibits Migration and Invasion of Human Glioblastoma Cells via Suppression Transforming Growth Factor β-Induced Epithelial-Mesenchymal Transition.

Zhaotao Wang, Zhi Liu, Guoyong Yu, Xiaohu Nie, Weiqiang Jia, Ru-En Liu, Ruxiang Xu

Open access · hybridAbstract read
In one paragraph

Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
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  6. The Role and Mechanism ofMolecules (Basel, Switzerland) · 2024
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  15. Paeoniflorin treatment regulates TLR4/NF-κB signaling, reduces cerebral oxidative stress and improves white matter integrity in neonatal hypoxic brain injury.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
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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 WangAffiliated Bayi Brain Hospital, General Army Hospital, Southern Medical University, Beijing, People's Republic of China.
Zhi LiuDepartment of Neurosurgery, Peking University People's Hospital, Peking University, Beijing, People's Republic of China.
Guoyong YuNanchang University Medical College, Nanchang, Jiangxi, People's Republic of China.
Xiaohu NieHuzhou Central Hospital, Zhejiang, People's Republic of China.
Weiqiang JiaAffiliated Bayi Brain Hospital, General Army Hospital, Southern Medical University, Beijing, People's Republic of China.
Ru-En LiuDepartment of Neurosurgery, Peking University People's Hospital, Peking University, Beijing, People's Republic of China. liuruen125@163.com.
Ruxiang XuAffiliated Bayi Brain Hospital, General Army Hospital, Southern Medical University, Beijing, People's Republic of China. xuruxiang81@163.com.
Southern Medical University · CNPeking University People's Hospital · CNHuzhou Central Hospital · CNNanchang University · CN

Funding

National Natural Science Foundation of China 81573774
6 · The paper itself

Abstract

Paeoniflorin (PF) is a polyphenolic compound derived from Radix Paeoniae Alba thathas anti-cancer activities in a variety of human malignancies including glioblastoma. However, the underlying mechanisms have not been fully elucidated. Epithelial to mesenchymal transition (EMT), characterized as losing cell polarity, plays an essential role in tumor invasion and metastasis. TGFβ, a key member of transforming growth factors, has been demonstrated to contribute to glioblastoma aggressiveness through inducing EMT. Therefore, the present studies aim to investigate whether PF suppresses the expression of TGFβ and inhibits EMT that plays an important role in anti-glioblastoma. We found that PF dose-dependently downregulates the expression of TGFβ, enhances apoptosis, reduces cell proliferation, migration and invasion in three human glioblastoma cell lines (U87, U251, T98G). These effects are enhanced in TGFβ siRNA treated cells and abolished in cells transfected with TGFβ lentiviruses. In addition, other EMT markers such as snail, vimentin and N-cadherin were suppressed by PF in these cell lines and in BALB/c nude mice injected with U87 cells. The expression of MMP2/9, EMT markers, are also dose-dependently reduced in PF treated cells and in U87 xenograft mouse model. Moreover, the tumor sizes are reduced by PF treatment while there is no change in body weight. These results indicate that PF is a potential novel drug target for the treatment of glioblastoma by suppression of TGFβ signaling pathway and inhibition of EMT.

Indexed as

AnimalsBrain NeoplasmsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticGlioblastomaGlucosidesGlycosidesHumansMice, NudeMonoterpenesNeoplasm InvasivenessTransforming Growth Factor betaGlucosidesGlycosidesMonoterpenespeoniflorinTransforming Growth Factor betaEMTGlioblastomaMigration and invasionPaeoniflorinTGFβ

Identifiers

PMID29423667
PMCPMC5842263
OpenAlexW2791556631

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.