Evidence map›Paper›PMID 30546442›Full record

ArticleOncology letters2018

Overexpression of HDAC6 suppresses tumor cell proliferation and metastasis by inhibition of the canonical Wnt/β-catenin signaling pathway in hepatocellular carcinoma.

Zhusheng Yin, Wei Xu, Hao Xu, Junnian Zheng, Yuming Gu

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Establishment of DNA Methylation Profile Associated with TCM Syndrome in Endometriosis.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  8. Article
  9. Article
  10. Histone deacetylase 2 polymorphisms associated with noise-induced hearing loss in Chinese workers.Environmental science and pollution research international · 2021
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

5 authors at 1 institution in 1 country.

Zhusheng YinDepartment of Interventional Radiology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221002, P.R. China.
Wei XuDepartment of Interventional Radiology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221002, P.R. China.
Hao XuDepartment of Interventional Radiology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221002, P.R. China.
Junnian ZhengJiangsu Key Laboratory of Biological Cancer Therapy, Xuzhou Medical University, Xuzhou, Jiangsu 221002, P.R. China.
Yuming GuDepartment of Interventional Radiology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221002, P.R. China.
Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylase 6 (HDAC6), a specific histone deacetylase family member, serves an essential role in the regulation of gene expression, cell cycle progression, autophagy and apoptosis. There are numerous reports on the function of HDAC6 in cancer. However, the specific function of HDAC6 in hepatocellular carcinoma (HCC) has yet to be revealed. In the present study, the expression of HDAC6 was revealed to be downregulated in human HCC cell lines and tissues. The aberrant activation of the canonical Wnt/β-catenin signaling pathway was revealed to be involved in hepatocarcinogenesis and metastasis. It was additionally revealed that the overexpression of HDAC6 decreased the expression of β-catenin protein levels which attenuated the canonical Wnt/β-catenin signaling pathway and suppressed the proliferation of HCC cells. In addition, the upregulation of HDAC6 inhibited the epithelial-to-mesenchymal transition in HCC by increasing the E-cadherin protein levels and decreasing the N-cadherin, vimentin and matrix metalloproteinase-9 protein levels. Furthermore, HDAC6 also exerted an effect on the cell cycle arrest and the induction of apoptosis. These results demonstrated that HDAC6 functioned as a tumor suppressor in HCC by attenuating the activity of the canonical Wnt/β-catenin signaling pathway. Therefore, HDAC6 may serve as a potential therapeutic target for the treatment of HCC.

Indexed as

epithelial-to-mesenchymal transitionhepatocellular carcinomahistone deacetylase 6Wntβ-catenin

Identifiers

PMID30546442
PMCPMC6256338
OpenAlexW2892931418

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.