Evidence map›Paper›PMID 21156786›Full record

ArticleMolecular cancer research : MCR2011

GT-094, a NO-NSAID, inhibits colon cancer cell growth by activation of a reactive oxygen species-microRNA-27a: ZBTB10-specificity protein pathway.

Satya S Pathi, Indira Jutooru, Gayathri Chadalapaka, Sandeep Sreevalsan, S Anand, Gregory Rj Thatcher, Stephen Safe

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 2 pooled it
8.3field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 111 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Specificity Proteins (Sp) and Cancer.International journal of molecular sciences · 2023
    Review
  5. Emerging role of miRNAs in the regulation of ferroptosis.Frontiers in molecular biosciences · 2023
    Review
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4 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Satya S PathiDepartment of Veterinary Physiology and Pharmacology, Texas A&M University, 4466 TAMU, Vet. Res. Bldg. 410, College Station, TX 77843, USA.
Indira Jutooru
Gayathri Chadalapaka
Sandeep Sreevalsan
S Anand
Gregory Rj Thatcher
Stephen Safe
Texas A&M University · USUniversity of Illinois Chicago · USTexas A&M Health Science Center · US

Funding

Biointeractions of Antiestrogens with Nitric OxideR01CA102590 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI THATCHER, GREGORY R. J · 2005 to 2015
$2.2M
Nitric Oxide Chimera Drugs for Colon Cancer ChemopreventionR01CA121107 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI THATCHER, GREGORY R. J · 2008 to 2012
$1.6M
MicroRNAs as Targets for Colon Cancer ChemotherapyR01CA136571 · NCI · TEXAS A&M UNIVERSITY · PI SAFE, STEPHEN H. · 2009 to 2013
$1.2M
NCI NIH HHS CA102590NCI NIH HHS CA136571NCI NIH HHS R01 CA102590NCI NIH HHS R01 CA121107NCI NIH HHS R01 CA136571
6 · The paper itself

Abstract

Ethyl 2-((2,3-bis(nitrooxy)propyl)disulfanyl)benzoate (GT-094) is a novel nitric oxide (NO) chimera containing an nonsteroidal anti-inflammatory drug (NSAID) and NO moieties and also a disulfide pharmacophore that in itself exhibits cancer chemopreventive activity. In this study, the effects and mechanism of action of GT-094 were investigated in RKO and SW480 colon cancer cells. GT-094 inhibited cell proliferation and induced apoptosis in both cell lines and this was accompanied by decreased mitochondrial membrane potential (MMP) and induction of reactive oxygen species (ROS), and these responses were reversed after cotreatment with the antioxidant glutathione. GT-094 also downregulated genes associated with cell growth [cyclin D1, hepatocyte growth factor receptor (c-Met), epidermal growth factor receptor (EGFR)], survival (bcl-2, survivin), and angiogenesis [VEGF and its receptors (VEGFR1 and VEGFR2)]. Results of previous RNA interference studies in this laboratory has shown that these genes are regulated, in part, by specificity protein (Sp) transcription factors Sp1, Sp3, and Sp4 that are overexpressed in colon and other cancer cell lines and not surprisingly, GT-094 also decreased Sp1, Sp3, and Sp4 in colon cancer cells. GT-094-mediated repression of Sp and Sp-regulated gene products was due to downregulation of microRNA-27a (miR-27a) and induction of ZBTB10, an Sp repressor that is regulated by miR-27a in colon cancer cells. Moreover, the effects of GT-094 on Sp1, Sp3, Sp4, miR-27a, and ZBTB10 were also inhibited by glutathione suggesting that the anticancer activity of GT-094 in colon cancer cells is due, in part, to activation of an ROS-miR-27a:ZBTB10-Sp transcription factor pathway.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalApoptosisCell Line, TumorCell ProliferationColonic NeoplasmsDisulfidesDNA-Binding ProteinsDown-RegulationDrug Screening Assays, AntitumorGene Expression Regulation, NeoplasticGlutathioneHumansMembrane Potential, MitochondrialMicroRNAsNeoplasm ProteinsNitratesAnti-Inflammatory Agents, Non-SteroidalDisulfidesDNA-Binding ProteinsGlutathioneGT 094MicroRNAsMIRN27 microRNA, humanNeoplasm ProteinsNitratesNitric OxideReactive Oxygen SpeciesRepressor ProteinsSp Transcription FactorsZBTB10 protein, human

Identifiers

PMID21156786
PMCPMC3069691
OpenAlexW2161176275

What OpenQuestion holds

Textmetadata
LicenceTDM
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.