Evidence map›Paper›PMID 29050320›Full record

ArticleOncotarget2017

Epigenetic regulation of interleukin-8 expression by class I HDAC and CBP in ovarian cancer cells.

Himavanth R Gatla, Yue Zou, Mohammad M Uddin, Ivana Vancurova

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Epigenetic regulation in gynecological cancers: a paradigm shift in immunotherapy strategies.Journal of experimental & clinical cancer research : CR · 2025
    Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. A secreted sirtuin fromScience advances · 2023
    Article
  7. Review
  8. Article
  9. Trained innate immunity, long-lasting epigenetic modulation, and skewed myelopoiesis by heme.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Review
  11. Review
  12. Article
  13. Combination Therapies Targeting HDAC and IKK in Solid Tumors.Trends in pharmacological sciences · 2018
    Review
  14. 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

4 authors at 2 institutions in 2 countries.

Himavanth R GatlaDepartment of Biological Sciences, St. John's University, New York City, NY 11439, USA.
Yue ZouDepartment of Biological Sciences, St. John's University, New York City, NY 11439, USA.
Mohammad M UddinDepartment of Biological Sciences, St. John's University, New York City, NY 11439, USA.
Ivana VancurovaDepartment of Biological Sciences, St. John's University, New York City, NY 11439, USA.
St. John's University · TWSt. John's University · US

Funding

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 CA202775
6 · The paper itself

Abstract

Although inhibitors of epigenetic regulators have been effective in the treatment of cutaneous T cell lymphoma (CTCL) and other hematopoietic malignancies, they have been less effective in solid tumors, including ovarian cancer (OC). We have previously shown that inhibition of histone deacetylase (HDAC) activity induces expression of the pro-inflammatory and pro-angiogenic chemokine interleukin-8 (CXCL8, IL-8) in OC cells, resulting in their increased survival and proliferation. Here, we show that in addition to ovarian cancer SKOV3, OVCAR3, and CAOV3 cells, HDAC inhibition induces the CXCL8 expression in HeLa cells, but not in CTCL Hut-78 cells. In OC cells, the CXCL8 expression is induced by pharmacological inhibition of class I HDACs. Interestingly, while an individual suppression of HDAC1, HDAC2, or HDAC3 by corresponding siRNAs inhibits the CXCL8 expression, their simultaneous suppression induces the CXCL8 expression. The induced CXCL8 expression in OC cells is dependent on histone acetyltransferase (HAT) activity of CREB-binding protein (CBP), but not p300, and is associated with HAT-dependent p65 recruitment to CXCL8 promoter. Together, our results show that the CXCL8 expression in OC cells is induced by combined inhibition of HDAC1, -2, and -3, and silenced by suppression of HAT activity of CBP. In addition, our data indicate that the induced CXCL8 expression may be responsible for the limited effectiveness of HDAC inhibitors in OC and perhaps other solid cancers characterized by CXCL8 overexpression, and suggest that targeting class I HDACs and CBP may provide novel combination strategies by limiting the induced CXCL8 expression.

Indexed as

CBPHDACinterleukin-8ovarian cancer

Identifiers

PMID29050320
PMCPMC5642595
OpenAlexW2744802799

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.