Evidence map›Paper›PMID 25226613›Full record

ArticleOncotarget2014

A novel action mechanism for MPT0G013, a derivative of arylsulfonamide, inhibits tumor angiogenesis through up-regulation of TIMP3 expression.

Chih-Ya Wang, Jing-Ping Liou, An-Chi Tsai, Mei-Jung Lai, Yi-Min Liu, Hsueh-Yun Lee, Jing-Chi Wang, Shiow-Lin Pan, Che-Ming Teng

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. Mechanisms of cardiovascular toxicity induced by PMEnvironmental science and pollution research international · 2021
    Review
  4. Article
  5. TIMP-3 as a therapeutic target for cancer.Therapeutic advances in medical oncology · 2019
    Review
  6. Article
  7. Article
  8. TIMP3 regulates osteosarcoma cell migration, invasion, and chemotherapeutic resistances.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  9. Article
  10. 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

9 authors at 2 institutions in 1 country.

Chih-Ya WangPharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan.
Jing-Ping LiouSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei, Taiwan.
An-Chi TsaiThe Ph.D. program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Mei-Jung LaiSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei, Taiwan.
Yi-Min LiuSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei, Taiwan.
Hsueh-Yun LeeSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei, Taiwan.
Jing-Chi WangThe Ph.D. program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Shiow-Lin PanThe Ph.D. program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Che-Ming TengPharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan.
Taipei Medical University · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tissue inhibitors of metalloproteinases 3 (TIMP3) were originally characterized as inhibitors of matrix metalloproteinases (MMPs), acting as potent antiangiogenic proteins. In this study, we demonstrated that the arylsulfonamide derivative MPT0G013 has potent antiangiogenic activities in vitro and in vivo viainducing TIMP3 expression. Treatments with MPT0G013 significantly inhibited endothelial cell functions, such as cell proliferation, migration, and tube formation, as well as induced p21 and cell cycle arrest at the G0/G1 phase. Subsequent microarray analysis showed significant induction of TIMP3 gene expression by MPT0G013, and siRNA-mediated blockage of TIMP3 up-regulation abrogated the antiangiogenic activities of MPT0G013 and prevented inhibition of p-AKT and p-ERK proteins. Importantly, MPT0G013 exhibited antiangiogenic activities in in vivo Matrigel plug assays, inhibited tumor growth and up-regulated TIMP3 and p21 proteins in HCT116 mouse xenograft models. These data suggest potential therapeutic application of MPT0G013 for angiogenesis-related diseases such as cancer.

Indexed as

Angiogenesis InhibitorsAnimalsApoptosisCell Cycle CheckpointsCell Line, TumorCell ProliferationColonic NeoplasmsFemaleG1 Phase Cell Cycle CheckpointsHCT116 CellsHumansHuman Umbilical Vein Endothelial CellsHydroxamic AcidsIndolesMaleMice3-(1-(3,4-dimethoxybenzenesulfonyl)-1H-indol-5-yl)-N-hydroxyacrylamideAngiogenesis InhibitorsHydroxamic AcidsIndolesTIMP3 protein, humanTissue Inhibitor of Metalloproteinase-3

Identifiers

PMID25226613
PMCPMC4259441
OpenAlexW1552807357

What OpenQuestion holds

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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.