Evidence map›Paper›PMID 20435036›Full record

ArticleExperimental cell research2010

Arsenic trioxide downregulates specificity protein (Sp) transcription factors and inhibits bladder cancer cell and tumor growth.

Indira Jutooru, Gayathri Chadalapaka, Sandeep Sreevalsan, Ping Lei, Rola Barhoumi, Robert Burghardt, Stephen Safe

Open access · greenAbstract read
In one paragraph

Article in Experimental cell research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Specificity Proteins (Sp) and Cancer.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Article
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  8. Review
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  16. Linkage Analysis of Urine Arsenic Species Patterns in the Strong Heart Family Study.Toxicological sciences : an official journal of the Society of Toxicology · 2015
    Article
  17. Article
  18. Article
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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 2 institutions in 1 country.

Indira JutooruDepartment of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, TX 77843-4466, USA. ijutooru@cvm.tamu.edu
Gayathri Chadalapaka
Sandeep Sreevalsan
Ping Lei
Rola Barhoumi
Robert Burghardt
Stephen Safe
Texas A&M University · USTexas A&M Health Science Center · US

Funding

MicroRNAs as Targets for Colon Cancer ChemotherapyR01CA136571 · NCI · TEXAS A&M UNIVERSITY · PI SAFE, STEPHEN H. · 2009 to 2013
$1.2M
NCI NIH HHS 5R01-CA136571NCI NIH HHS R01 CA136571
6 · The paper itself

Abstract

Arsenic trioxide exhibits antiproliferative, antiangiogenic and proapoptotic activity in cancer cells, and many genes associated with these responses are regulated by specificity protein (Sp) transcription factors. Treatment of cancer cells derived from urologic (bladder and prostate) and gastrointestinal (pancreas and colon) tumors with arsenic trioxide demonstrated that these cells exhibited differential responsiveness to the antiproliferative effects of this agent and this paralleled their differential repression of Sp1, Sp3 and Sp4 proteins in the same cell lines. Using arsenic trioxide-responsive KU7 and non-responsive 253JB-V bladder cancer cells as models, we show that in KU7 cells, < or =5 microM arsenic trioxide decreased Sp1, Sp3 and Sp4 and several Sp-dependent genes and responses including cyclin D1, epidermal growth factor receptor, bcl-2, survivin and vascular endothelial growth factor, whereas at concentrations up to 15 microM, minimal effects were observed in 253JB-V cells. Arsenic trioxide also inhibited tumor growth in athymic mice bearing KU7 cells as xenografts, and expression of Sp1, Sp3 and Sp4 was significantly decreased. Inhibitors of oxidative stress such as glutathione or dithiothreitol protected KU7 cells from arsenic trioxide-induced antiproliferative activity and Sp repression, whereas glutathione depletion sensitized 253JB-V cells to arsenic trioxide. Mechanistic studies suggested that arsenic trioxide-dependent downregulation of Sp and Sp-dependent genes was due to decreased mitochondrial membrane potential and induction of reactive oxygen species, and the role of peroxides in mediating these responses was confirmed using hydrogen peroxide.

Indexed as

AnimalsAntineoplastic AgentsApoptosisArsenicalsArsenic TrioxideBlotting, WesternCell ProliferationDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansMiceMice, NudeOxidesReactive Oxygen SpeciesReverse Transcriptase Polymerase Chain ReactionAntineoplastic AgentsArsenicalsArsenic TrioxideOxidesReactive Oxygen SpeciesRNA, MessengerSp Transcription Factors

Identifiers

PMID20435036
PMCPMC2900380
OpenAlexW2024885145

What OpenQuestion holds

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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.