Evidence map›Paper›PMID 23724067›Full record

ArticlePloS one2013

HDAC up-regulation in early colon field carcinogenesis is involved in cell tumorigenicity through regulation of chromatin structure.

Yolanda Stypula-Cyrus, Dhwanil Damania, Dhananjay P Kunte, Mart Dela Cruz, Hariharan Subramanian, Hemant K Roy, Vadim Backman

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

77 citing papers in PubMed, 138 citations in OpenAlex.

  1. Whole Exome Sequencing IdentifiesInternational journal of molecular sciences · 2021
    Trial
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  7. Review
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  12. HDAC7: a promising target in cancer.Frontiers in oncology · 2024
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Frontiers in microbiology · 2023
    Article
  19. HDAC2 as a target for developing anti-cancer drugs.Computational and structural biotechnology journal · 2023
    Review
  20. Article

17 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.

Yolanda Stypula-CyrusBiomedical Engineering Department, Northwestern University, Evanston, Illinois, United States of America.
Dhwanil Damania
Dhananjay P Kunte
Mart Dela Cruz
Hariharan Subramanian
Hemant K Roy
Vadim Backman
Northwestern University · USBoston Medical Center · USNorthShore University HealthSystem · US

Funding

TRANS-NETWORK PROJECTSU54CA143869 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WIDOM, JONATHAN · 2009 to 2013
$12.8M
Novel Biophotonics Methodology for Colon Cancer ScreeningR01CA128641 · NCI · NORTHWESTERN UNIVERSITY · PI BACKMAN, VADIM · 2008 to 2012
$7.3M
NCI NIH HHS R01 CA128641NCI NIH HHS R01CA128641NCI NIH HHS U54 CA143869NCI NIH HHS U54CA143869
6 · The paper itself

Abstract

Normal cell function is dependent on the proper maintenance of chromatin structure. Regulation of chromatin structure is controlled by histone modifications that directly influence chromatin architecture and genome function. Specifically, the histone deacetylase (HDAC) family of proteins modulate chromatin compaction and are commonly dysregulated in many tumors, including colorectal cancer (CRC). However, the role of HDAC proteins in early colorectal carcinogenesis has not been previously reported. We found HDAC1, HDAC2, HDAC3, HDAC5, and HDAC7 all to be up-regulated in the field of human CRC. Furthermore, we observed that HDAC2 up-regulation is one of the earliest events in CRC carcinogenesis and observed this in human field carcinogenesis, the azoxymethane-treated rat model, and in more aggressive colon cancer cell lines. The universality of HDAC2 up-regulation suggests that HDAC2 up-regulation is a novel and important early event in CRC, which may serve as a biomarker. HDAC inhibitors (HDACIs) interfere with tumorigenic HDAC activity; however, the precise mechanisms involved in this process remain to be elucidated. We confirmed that HDAC inhibition by valproic acid (VPA) targeted the more aggressive cell line. Using nuclease digestion assays and transmission electron microscopy imaging, we observed that VPA treatment induced greater changes in chromatin structure in the more aggressive cell line. Furthermore, we used the novel imaging technique partial wave spectroscopy (PWS) to quantify nanoscale alterations in chromatin. We noted that the PWS results are consistent with the biological assays, indicating a greater effect of VPA treatment in the more aggressive cell type. Together, these results demonstrate the importance of HDAC activity in early carcinogenic events and the unique role of higher-order chromatin structure in determining cell tumorigenicity.

Indexed as

Up-RegulationAnimalsCarcinogenesisCell SurvivalChromatinColorectal NeoplasmsHistone Deacetylase InhibitorsHistone DeacetylasesHT29 CellsHumansIntestinal MucosaRatsRats, Inbred F344Spectrum AnalysisValproic AcidChromatinHistone Deacetylase InhibitorsHistone DeacetylasesValproic Acid

Identifiers

PMID23724067
PMCPMC3665824
OpenAlexW2013870404

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.