Evidence map›Paper›PMID 21151670›Full record

ReviewJournal of biomedicine & biotechnology2011

Histone deacetylase inhibitors: the epigenetic therapeutics that repress hypoxia-inducible factors.

Shuyang Chen, Nianli Sang

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of biomedicine & biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.2field-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

41 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
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  13. Article
  14. Valproic acid inhibits the angiogenic potential of cervical cancer cells via HIF-1α/VEGF signals.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2016
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. The role of inflammation in hypoxic pulmonary hypertension: from cellular mechanisms to clinical phenotypes.American journal of physiology. Lung cellular and molecular physiology · 2015
    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

2 authors at 1 institution in 1 country.

Shuyang ChenDepartment of Biology and Graduate Program of Biological Sciences, College of Arts & Sciences, Drexel University, 3141 Chestnut Street, Stratton Hall 318, Philadelphia, PA 19104, USA.
Nianli Sang
Drexel University · US

Funding

Repressing HIF-1: targets and mechanismsR01CA129494 · NCI · DREXEL UNIVERSITY · PI SANG, NIANLI · 2008 to 2012
$1.6M
Transactivating of Activity of HIF-1 in tumorigenesisK01CA098809 · NCI · THOMAS JEFFERSON UNIVERSITY · PI SANG, NIANLI · 2003 to 2007
$714k
NCI NIH HHS K01 CA098809NCI NIH HHS K01-CA098809NCI NIH HHS R01 CA129494NCI NIH HHS R01-CA129494
6 · The paper itself

Abstract

Histone deacetylase inhibitors (HDACIs) have been actively explored as a new generation of chemotherapeutics for cancers, generally known as epigenetic therapeutics. Recent findings indicate that several types of HDACIs repress angiogenesis, a process essential for tumor metabolism and progression. Accumulating evidence supports that this repression is mediated by disrupting the function of hypoxia-inducible factors (HIF-1, HIF-2, and collectively, HIF), which are the master regulators of angiogenesis and cellular adaptation to hypoxia. Since HIF also regulate glucose metabolism, cell survival, microenvironment remodeling, and other alterations commonly required for tumor progression, they are considered as novel targets for cancer chemotherapy. Though the precise biochemical mechanism underlying the HDACI-triggered repression of HIF function remains unclear, potential cellular factors that may link the inhibition of deacetylase activity to the repression of HIF function have been proposed. Here we review published data that inhibitors of type I/II HDACs repress HIF function by either reducing functional HIF-1α levels, or repressing HIF-α transactivation activity. In addition, underlying mechanisms and potential proteins involved in the repression will be discussed. A thorough understanding of HDACI-induced repression of HIF function may facilitate the development of future therapies to either repress or promote angiogenesis for cancer or chronic ischemic disorders, respectively.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1EpigenomicsHistone Deacetylase InhibitorsHumansHypoxia-Inducible Factor 1Basic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1Histone Deacetylase InhibitorsHypoxia-Inducible Factor 1

Identifiers

PMID21151670
PMCPMC2997513
OpenAlexW1987912212

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.