Evidence map›Paper›PMID 28167529›Full record

ArticleThe Journal of biological chemistry2017

Histone Deacetylase (HDAC) Inhibition Induces IκB Kinase (IKK)-dependent Interleukin-8/CXCL8 Expression in Ovarian Cancer Cells.

Himavanth R Gatla, Yue Zou, Mohammad M Uddin, Bipradeb Singha, Pengli Bu, Ales Vancura, Ivana Vancurova

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Epigenetic regulation in gynecological cancers: a paradigm shift in immunotherapy strategies.Journal of experimental & clinical cancer research : CR · 2025
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  11. Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  12. Diverse Epigenetic Regulations of Macrophages in Atherosclerosis.Frontiers in cardiovascular medicine · 2022
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  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 1 country.

Himavanth R GatlaFrom the Department of Biological Sciences, St. John's University, New York, New York 11439 and.
Yue ZouFrom the Department of Biological Sciences, St. John's University, New York, New York 11439 and.
Mohammad M UddinFrom the Department of Biological Sciences, St. John's University, New York, New York 11439 and.
Bipradeb SinghaThe Wistar Institute, Philadelphia, Pennsylvania 19104.
Pengli BuFrom the Department of Biological Sciences, St. John's University, New York, New York 11439 and.
Ales VancuraFrom the Department of Biological Sciences, St. John's University, New York, New York 11439 and.
Ivana VancurovaFrom the Department of Biological Sciences, St. John's University, New York, New York 11439 and vancuroi@stjohns.edu.
St. John's University · USThe Wistar Institute · US

Funding

Interleukin-8 Regulation by Proteasome and Nuclear IkB in Cancer and InflammationR15CA173452 · NCI · ST. JOHN'S UNIVERSITY · PI VANCUROVA, IVANA · 2013 to 2013
$495k
Targeting IKK and HDAC Mediated IL-8 Expression in Ovarian and Prostate CancerR15CA202775 · NCI · ST. JOHN'S UNIVERSITY · PI VANCUROVA, IVANA · 2016 to 2016
$495k
NCI NIH HHS R15 CA173452NCI NIH HHS R15 CA202775
6 · The paper itself

Abstract

Overexpression of the pro-angiogenic chemokine IL-8 (CXCL8) is associated with a poor prognosis in several solid tumors, including epithelial ovarian cancer (EOC). Even though histone deacetylase (HDAC) inhibition has shown remarkable antitumor activity in hematological malignancies, it has been less effective in solid tumors, including EOC. Here we report results that may explain the decreased efficiency of HDAC inhibition in EOC, based on our data demonstrating that HDAC inhibition specifically induces expression of IL-8/CXCL8 in SKOV3, CAOV3, and OVCAR3 cells. Suppression or neutralization of vorinostat-induced IL-8/CXCL8 potentiates the vorinostat inhibitory effect on cell viability and proliferation. The IL-8/CXCL8 expression induced by vorinostat in EOC cells is dependent on IκB kinase (IKK) activity and associated with a gene-specific recruitment of IKKβ and IKK-dependent recruitment of p65 NFκB to the IL-8/CXCL8 promoter. In addition, HDAC inhibition induces acetylation of p65 and histone H3 and their IL-8/CXCL8 promoter occupancy.

Indexed as

AcetylationAnimalsAntineoplastic AgentsApoptosisFemaleHistone Deacetylase InhibitorsHumansHydroxamic AcidsI-kappa B KinaseInterleukin-8Mice, NudeOvarian NeoplasmsOvaryPromoter Regions, GeneticUp-RegulationVorinostatAntineoplastic AgentsHistone Deacetylase InhibitorsHydroxamic AcidsI-kappa B KinaseInterleukin-8VorinostatchemokineCXCL8histone deacetylase (HDAC)histone deacetylase inhibitor (HDI)interleukininterleukin-8IκB kinaseovarian cancer

Identifiers

PMID28167529
PMCPMC5377816
OpenAlexW2586167592

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.