Evidence map›Paper›PMID 17923479›Full record

ArticleThe Journal of biological chemistry2007

Inhibition of histone deacetylase activity promotes invasion of human cancer cells through activation of urokinase plasminogen activator.

Sai Murali Krishna Pulukuri, Bharathi Gorantla, Jasti S Rao

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in The Journal of biological chemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. New and emerging HDAC inhibitors for cancer treatment.The Journal of clinical investigation · 2014
    Review
  14. Article
  15. Article
  16. Histone deacetylases and cancer.Molecular oncology · 2012
    Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Sai Murali Krishna PulukuriDepartment of Cancer Biology, University of Illinois College of Medicine, Peoria, Illinois 61656, USA.
Bharathi Gorantla
Jasti S Rao
University of Illinois Urbana-Champaign · US

Funding

Cath B and uPAR si RNA constructs regressed glioma growthR01CA116708 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI O'BRYAN, JOHN P · 2005 to 2014
$2.9M
Inhibition of glioma tumor growth by antisense MMP-9R01NS047699 · NINDS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAO, JASTI S. · 2003 to 2011
$2.5M
Role of uPA and uPAR in Human Glioma InvasivenessR01CA075557 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI RAO, JASTI S. · 1998 to 2009
$2.3M
Growth inhibition of brain tumors by cord blood stem cellsR01NS057529 · NINDS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAO, JASTI S. · 2006 to 2010
$1.8M
Role of TFPI-2 in human gliomas invasivenessR01CA095058 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAO, JASTI S. · 2003 to 2007
$1.5M
Suppression of glioma invasion by a bicistronic constuctR01CA092393 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAO, JASTI S. · 2003 to 2007
$1.4M
NCI NIH HHS CA116708NCI NIH HHS CA75557NCI NIH HHS CA92393NCI NIH HHS CA95058NCI NIH HHS R01 CA075557NCI NIH HHS R01 CA092393NCI NIH HHS R01 CA095058NCI NIH HHS R01 CA116708NINDS NIH HHS NS057529NINDS NIH HHS NS47699NINDS NIH HHS R01 NS047699NINDS NIH HHS R01 NS057529
6 · The paper itself

Abstract

Histone acetylation plays an important role in chromatin remodeling and gene expression. The molecular mechanisms involved in differential regulation of urokinase plasminogen activator (uPA) gene expression are not fully understood. In this study, we investigated whether histone deacetylation was involved in repression of uPA expression in human cancer cells. Induction of uPA expression by histone deacetylase (HDAC) inhibitors trichostatin A (TSA), sodium butyrate, and scriptaid was observed in all three different types of human cancer cells examined. Chromatin immunoprecipitation assays showed that the induction of uPA expression by TSA was accompanied by a remarkable increase of acetylation of histones H3 and H4, which are associated with the uPA promoter region in human cancer cells. These results were further substantiated by the findings of a restriction enzyme accessibility assay and TSA-stimulated uPA promoter activity through the inhibition of HDAC activity. In vitro Matrigel invasion assays showed that induction of uPA expression by HDAC inhibitors in human cancer cells resulted in a significant increase of cancer cell invasion. Furthermore, HDAC1 knockdown by small interference RNA stimulated uPA expression and cancer cell invasion. In conclusion, this study demonstrates the important role of histone modifications in regulating uPA gene expression and raises a possibility that the use of HDAC inhibitors in patients as cancer therapy may paradoxically establish metastasis through up-regulation or reactivation of uPA.

Indexed as

Gene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticButyratesCell Line, TumorEnzyme ActivationEnzyme InhibitorsHistone Deacetylase 1Histone Deacetylase InhibitorsHistone DeacetylasesHistonesHumansHydroxamic AcidsNeoplasm InvasivenessNeoplasm MetastasisNeoplasm ProteinsNeoplasmsButyratesEnzyme InhibitorsHDAC1 protein, humanHistone Deacetylase 1Histone Deacetylase InhibitorsHistone DeacetylasesHistonesHydroxamic AcidsNeoplasm ProteinsRNA, Small Interferingtrichostatin AUrokinase-Type Plasminogen Activator

Identifiers

PMID17923479
PMCPMC2156646
OpenAlexW2144699624

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.