Evidence map›Paper›PMID 26508835›Full record

ArticleDrug design, development and therapy2015

Paeoniflorin inhibits human glioma cells via STAT3 degradation by the ubiquitin-proteasome pathway.

Xiao-hu Nie, Jia Ou-yang, Ying Xing, Dan-yan Li, Xing-yu Dong, Ru-en Liu, Ru-xiang Xu

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

29 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. The Small Molecules of Plant Origin with Anti-Glioma Activity.International journal of molecular sciences · 2025
    Review
  4. Article
  5. The Role and Mechanism ofMolecules (Basel, Switzerland) · 2024
    Review
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  16. Article
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  19. Kuijieling-Containing Serum Regulates Th17 and Treg Cell Differentiation by Inhibiting STAT3 SignalingEvidence-based complementary and alternative medicine : eCAM · 2019
    Article
  20. Article
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 1 institution in 1 country.

Xiao-hu NieAffiliated Bayi Brain Hospital, Southern Medical University, Beijing, People's Republic of China.
Jia Ou-yangNanchang University Medical College, Jiangxi, People's Republic of China.
Ying XingDepartment of Gastroenterology, The 98th Hospital of Nanjing Military Command, Huzhou, Zhejiang, People's Republic of China.
Dan-yan LiSpleen & Stomach Institution, Guangzhou University of Traditional Chinese Medicine, Guangdong, People's Republic of China.
Xing-yu DongAffiliated Bayi Brain Hospital, Southern Medical University, Beijing, People's Republic of China.
Ru-en LiuDepartment of Neurosurgery, China-Japan Friendship Hospital, Beijing, People's Republic of China.
Ru-xiang XuBayi Brain Hospital, The Military General Hospital of Beijing PLA, Beijing, People's Republic of China.
China-Japan Friendship Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the underlying mechanism for the potent proapoptotic effect of paeoniflorin (PF) on human glioma cells in vitro, focusing on signal transducer and activator of transcription 3 (STAT3) signaling. Significant time- and dose-dependent apoptosis and inhibition of proliferation were observed in PF-treated U87 and U251 glioma cells. Expression of STAT3, its active form phosphorylated STAT3 (p-STAT3), and several downstream molecules, including HIAP, Bcl-2, cyclin D1, and Survivin, were significantly downregulated upon PF treatment. Overexpression of STAT3 induced resistance to PF, suggesting that STAT3 was a critical target of PF. Interestingly, rapid downregulation of STAT3 was consistent with its accelerated degradation, but not with its dephosphorylation or transcriptional modulation. Using specific inhibitors, we demonstrated that the prodegradation effect of PF on STAT3 was mainly through the ubiquitin-proteasome pathway rather than via lysosomal degradation. These findings indicated that PF-induced growth suppression and apoptosis in human glioma cells through the proteasome-dependent degradation of STAT3.

Indexed as

Antineoplastic Agents, PhytogenicApoptosisBrain NeoplasmsCell Line, TumorCell ProliferationDose-Response Relationship, DrugGliomaGlucosidesGlycosidesHumansMonoterpenesPhosphorylationProteasome Endopeptidase ComplexProteolysisSignal TransductionSTAT3 Transcription FactorAntineoplastic Agents, PhytogenicGlucosidesGlycosidesMonoterpenespeoniflorinProteasome Endopeptidase ComplexSTAT3 protein, humanSTAT3 Transcription FactorUbiquitinapoptosisgliomapaeoniflorinproliferationsignal transducer and activator of transcription 3 (STAT3)ubiquitin–proteasome pathway (UPP)

Identifiers

PMID26508835
PMCPMC4610779
OpenAlexW1958310212

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.