Evidence map›Paper›PMID 27283490›Full record

ArticleOncotarget2017

Aryl hydrocarbon receptor regulates histone deacetylase 8 expression to repress tumor suppressive activity in hepatocellular carcinoma.

Li-Ting Wang, Shyh-Shin Chiou, Chee-Yin Chai, Edward Hsi, Shen-Nien Wang, Shau-Ku Huang, Shih-Hsien Hsu

Erratum issuedOpen 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. An erratum has been issued. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. The aryl hydrocarbon receptor: a new frontier in male reproductive system.Reproductive biology and endocrinology : RB&E · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Histone Modifications in NAFLD: Mechanisms and Potential Therapy.International journal of molecular sciences · 2023
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. DNA Methylation Patterns inEnvironmental health perspectives · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. TCDD Toxicity Mediated by Epigenetic Mechanisms.International journal of molecular sciences · 2018
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Li-Ting WangGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
Shyh-Shin ChiouDepartment of Pediatrics, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
Chee-Yin ChaiDepartment of Pathology, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
Edward HsiDepartment of Genome Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
Shen-Nien WangGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
Shau-Ku HuangDivision of Environmental Health and Occupational Medicine, National Health Research Institutes, Zhunan 115, Taiwan.
Shih-Hsien HsuGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
Kaohsiung Medical University · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TWNational Health Research Institutes · TW

Funding

HSRD VA CDA 10-014
6 · The paper itself

Abstract

Histone deacetylase 8 (HDAC8), a unique member of class I histone deacetylases, shows remarkable correlation with advanced disease stage and multiple malignant tumors However, little is known about the contribution of HDAC8 to the tumorigenesis of hepatocellular carcinoma (HCC). The present study investigated the expression of HDAC8 regulated by the aryl hydrocarbon receptor (AHR) in HCC cell lines and tissues, and the roles of HDAC8 overexpression in cell proliferation, including potentially underlying mechanisms. We assessed the correlation between the clinic-pathological parameters and the expression of AHR and HDAC8. Further, we analyzed the AHR siRNA transfection and HDAC8 inhibitors to explore the functions of HDAC8 in HCC progression in vitro and in vivo. In a panel of 289 HCC patients, HDAC8 was shown to be highly correlated with AHR expression at both mRNA and protein levels. HCC patients with high AHR expression showed a shorter survival time than that with low AHR expression. We then found that the expression of both AHR and HDAC8 was significantly upregulated in both HCC cell lines and tumor tissues compared to human normal hepatocytes and matched non-tumor tissues. Furthermore, HDAC8 inhibition remarkably inhibited hepatoma cell proliferation and transformation activity via upregulation of RB1 in vitro and in vivo. Our data revealed an important role of the AHR-HDAC8 axis in promoting HCC tumorigenesis, thus identifying HDAC8 as a potential therapeutic target for HCC treatment.

Indexed as

Cell ProliferationAgedAnimalsAntineoplastic AgentsBasic Helix-Loop-Helix ProteinsBinding SitesCarcinoma, HepatocellularFemaleGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHep G2 CellsHistone Deacetylase InhibitorsHistone DeacetylasesHumansKaplan-Meier EstimateLiver NeoplasmsAHR protein, humanAntineoplastic AgentsBasic Helix-Loop-Helix ProteinsHDAC8 protein, humanHistone Deacetylase InhibitorsHistone DeacetylasesRB1 protein, humanReceptors, Aryl HydrocarbonRepressor ProteinsRetinoblastoma Binding ProteinsUbiquitin-Protein LigasesAHRHDAC8hepatocellular carcinoma (HCC)

Identifiers

PMID27283490
PMCPMC5352337
OpenAlexW2415633949

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.