Evidence map›Paper›PMID 23580655›Full record

ArticleThe Journal of biological chemistry2013

Wedelolactone, a naturally occurring coumestan, enhances interferon-γ signaling through inhibiting STAT1 protein dephosphorylation.

Zhimin Chen, Xiaoxiao Sun, Shensi Shen, Haohao Zhang, Xiuquan Ma, Jingli Liu, Shan Kuang, Qiang Yu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Journal of biomedical research & environmental sciences · 2022
    Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Wedelolactone from VietnameseIranian journal of pharmaceutical research : IJPR · 2018
    Article
  11. Review
  12. Wedelolactone Acts as Proteasome Inhibitor in Breast Cancer Cells.International journal of molecular sciences · 2017
    Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. 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

8 authors at 2 institutions in 1 country.

Zhimin ChenShanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203 Shanghai, China.
Xiaoxiao SunShanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203 Shanghai, China.
Shensi ShenShanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203 Shanghai, China.
Haohao ZhangShanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203 Shanghai, China.
Xiuquan MaShanghai Institute of Organic Chemistry, Chinese Academy of Sciences, 201203 Shanghai, China.
Jingli LiuShanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203 Shanghai, China.
Shan KuangShanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203 Shanghai, China.
Qiang YuShanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203 Shanghai, China. Electronic address: qyu@sibs.ac.cn.
Chinese Academy of Sciences · CNShanghai Institute of Materia Medica · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signal transducers and activators of transcription 1 (STAT1) transduces signals from cytokines and growth factors, particularly IFN-γ, and regulates expression of genes involved in cell survival/death, proliferation, and migration. STAT1 is activated through phosphorylation on its tyrosine 701 by JAKs and is inactivated through dephosphorylation by tyrosine phosphatases. We discovered a natural compound, wedelolactone, that increased IFN-γ signaling by inhibiting STAT1 dephosphorylation and prolonging STAT1 activation through specific inhibition of T-cell protein tyrosine phosphatase (TCPTP), an important tyrosine phosphatase for STAT1 dephosphorylation. More interestingly, wedelolactone inhibited TCPTP through interaction with the C-terminal autoinhibition domain of TCPTP. We also found that wedelolactone synergized with IFN-γ to induce apoptosis of tumor cells. Our data suggest a new target for anticancer or antiproliferation drugs, a new mechanism to regulate PTPs specifically, and a new drug candidate for treating cancer or other proliferation disorders.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic AgentsCell Line, TumorCell SurvivalCoumarinsDrug Screening Assays, AntitumorGenes, ReporterHep G2 CellsHumansInterferon-gammaPhosphoric Monoester HydrolasesPhosphorylationPlant ExtractsPromoter Regions, GeneticRNA InterferenceSTAT1 Transcription FactorAntineoplastic AgentsCoumarinscoumestanInterferon-gammaPhosphoric Monoester HydrolasesPlant ExtractsSTAT1 protein, humanSTAT1 Transcription FactorwedelolactoneCytokines/InterferonPhosphataseSTAT Transcription FactorTumor Suppressor GeneTumor Therapy

Identifiers

PMID23580655
PMCPMC3656297
OpenAlexW2066617235

What OpenQuestion holds

Textmetadata
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.