Evidence map›Paper›PMID 20531301›Full record

ArticleOncogene2010

Inhibition of AP-1 by SARI negatively regulates transformation progression mediated by CCN1.

R Dash, Z-Z Su, S-G Lee, B Azab, H Boukerche, D Sarkar, P B Fisher

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

32 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
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  11. Identification of prognostic immune genes in laryngeal cancer.The Journal of international medical research · 2020
    Article
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    Article
  13. Observational
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  18. Review
  19. Review
  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 2 institutions in 3 countries.

R DashDepartment of Human and Molecular Genetics, School of Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Z-Z Su
S-G Lee
B Azab
H Boukerche
D Sarkar
P B Fisher
Virginia Commonwealth University · USKyung Hee University · KR

Funding

Translational Applications of mda-7/IL-24 in CancerP01CA104177 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI FISHER, PAUL B · 2005 to 2009
$6.5M
MDA-7: Novel Cancer Therapeutic GeneR01CA097318 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI FISHER, PAUL B · 2002 to 2012
$2.8M
NCI NIH HHS P01 CA104177NCI NIH HHS R01 CA097318
6 · The paper itself

Abstract

Enhanced expression of the CCN family of secretory integrin-binding proteins correlates with many essential components of the cancerous state, including tumor cell adhesion, proliferation, invasion and migration. Consequently, CCN1 expression is elevated in various cancers, including breast cancer, and its expression directly correlates with poor patient prognosis. Using subtraction-hybridization, combined with induction of cancer cell terminal differentiation, we cloned SARI (suppressor of activator protein (AP)-1, regulated by interferon (IFN)), an IFN-beta-inducible, potent tumor suppressor gene that exerts cancer-selective growth inhibitory effects. Forced expression of SARI using an adenovirus (Ad.SARI) inhibits AP-1 function and downregulates CCN1 expression in multiple cancer lineages, resulting in a profound inhibition in anchorage-independent cell growth and tumor cell invasion. Overexpression of SARI reduces CCN1-promoter activity through inhibition of AP-1 binding. Accordingly, SARI selectively blocks expression of the transformed state in rat embryo fibroblast cells that stably overexpress c-Jun. These results illustrate that SARI inhibits AP-1 transactivating factor binding to the cis-element of the CCN1 promoter, possibly through its interaction with c-Jun. Overall, SARI can directly inhibit CCN1-induced transformation by inhibiting the transcription of CCN1, as well as indirectly by inhibiting the expression of c-Jun (and hence blocking AP-1 activity). In these contexts, transformed cells 'addicted' to AP-1 activity are rendered susceptible to SARI-mediated inhibition of expression of the transformed phenotype.

Indexed as

AnimalsCell AdhesionCell ProliferationCell Transformation, NeoplasticCysteine-Rich Protein 61Disease ProgressionGenes, Tumor SuppressorHumansMiceMice, NudeNeoplasm InvasivenessRatsTranscription Factor AP-1TransfectionTumor Cells, CulturedTumor Suppressor ProteinsCysteine-Rich Protein 61Transcription Factor AP-1Tumor Suppressor Proteins

Identifiers

PMID20531301
OpenAlexW1974322692

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.