Evidence map›Paper›PMID 22970280›Full record

ArticlePloS one2012

Transcriptional and epigenetic regulation of KIAA1199 gene expression in human breast cancer.

Cem Kuscu, Nikki Evensen, Deborah Kim, You-Jun Hu, Stanley Zucker, Jian Cao

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

38 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. The crucial role of CEMIP in cancer metastasis: Mechanistic insights and clinical implications.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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  11. Article
  12. International journal of medical sciences · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. TMEM2: A missing link in hyaluronan catabolism identified?Matrix biology : journal of the International Society for Matrix Biology · 2019
    Review
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

6 authors at 1 institution in 1 country.

Cem KuscuDepartment of Medicine/Cancer Prevention, Stony Brook University, Stony Brook, New York, United States of America.
Nikki Evensen
Deborah Kim
You-Jun Hu
Stanley Zucker
Jian Cao
Stony Brook University · US

Funding

Targeting the PEX Domain of MT1-MMP: Novel Cancer TherapyR01CA113553 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI CAO, JIAN · 2006 to 2010
$1.7M
Integrating Anti-invasive and Anti-growth Therapies Targeting Cancer MetastasisR01CA166936 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI SAMPSON, NICOLE S · 2012 to 2016
$1.6M
NCI NIH HHS R01 CA113553NCI NIH HHS R01CA113553NCI NIH HHS R01 CA166936NCI NIH HHS R01CA166936
6 · The paper itself

Abstract

Emerging evidence has demonstrated that upregulated expression of KIAA1199 in human cancer bodes for poor survival. The regulatory mechanism controlling KIAA1199 expression in cancer remains to be characterized. In the present study, we have isolated and characterized the human KIAA1199 promoter in terms of regulation of KIAA1199 gene expression. A 3.3 kb fragment of human genomic DNA containing the 5'-flanking sequence of the KIAA1199 gene possesses both suppressive and activating elements. Employing a deletion mutagenesis approach, a 1.4 kb proximal region was defined as the basic KIAA1199 promoter containing a TATA-box close to the transcription start site. A combination of 5'-primer extension study with 5'RACE DNA sequencing analysis revealed one major transcription start site that is utilized in the human KIAA1199 gene. Bioinformatics analysis suggested that the 1.4 kb KIAA1199 promoter contains putative activating regulatory elements, including activator protein-1(AP-1), Twist-1, and NF-κB sites. Sequential deletion and site-direct mutagenesis analysis demonstrated that the AP-1 and distal NF-κB sites are required for KIAA1199 gene expression. Further analyses using an electrophoretic mobility-shift assay and chromatin immunoprecipitation confirmed the requirement of these cis- and trans-acting elements in controlling KIAA1199 gene expression. Finally, we found that upregulated KIAA1199 expression in human breast cancer specimens correlated with hypomethylation of the regulatory region. Involvement of DNA methylation in regulation of KIAA1199 expression was recapitulated in human breast cancer cell lines. Taken together, our study unraveled the regulatory mechanisms controlling KIAA1199 gene expression in human cancer.

Indexed as

Epigenesis, GeneticTranscription, GeneticBase SequenceBreast NeoplasmsDNAFemaleGene SilencingHumansHyaluronoglucosaminidaseMolecular Sequence DataPromoter Regions, GeneticProteinsReal-Time Polymerase Chain ReactionSequence Homology, Nucleic AcidCEMIP protein, humanDNAHyaluronoglucosaminidaseProteins

Identifiers

PMID22970280
PMCPMC3435267
OpenAlexW2021884121

What OpenQuestion holds

Textmetadata
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.