Evidence map›Paper›PMID 28004105›Full record

ArticleInternational journal of molecular medicine2017

UHRF2 decreases H3K9ac expression by interacting with it through the PHD and SRA/YDG domain in HepG2 hepatocellular carcinoma cells.

Ting Zhang, Linglin Zhao, Shengyuan Zeng, Lu Bai, Junxia Chen, Zheng Zhang, Yalan Wang, Changzhu Duan

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. E3 Ubiquitin LigaseInternational journal of molecular sciences · 2024
    Article
  5. Article
  6. The roles of E3 ligases in Hepatocellular carcinoma.American journal of cancer research · 2022
    Review
  7. 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

8 authors at 1 institution in 1 country.

Ting ZhangMolecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, P.R. China.
Linglin ZhaoMolecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, P.R. China.
Shengyuan ZengMolecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, P.R. China.
Lu BaiMolecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, P.R. China.
Junxia ChenMolecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, P.R. China.
Zheng ZhangMolecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, P.R. China.
Yalan WangMolecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, P.R. China.
Changzhu DuanMolecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, P.R. China.
Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ubiquitin-like with PHD and ring finger domains 2 (UHRF2) is a multi-domain E3 ubiquitin ligase which is involved in epigenetic regulation and plays an essential role in tumorigenesis. However, the role of UHRF2 in histone H3 acetylation has not yet been fully elucidated and few studies have reported its role in hepatocellular carcinoma (HCC). In this study, we examined the correlation between UHRF2 and acetylated H3 in HCC. Immunohistochemistry and western blot analysis demonstrated that the levels of histone H3 lysine 9 acetylation (H3K9ac) and histone H3 lysine 14 acetylation (H3K14ac) were higher in the HCC tissues and HepG2 HCC cells compared with the adjacent non-tumor tissues and L02 normal cells. The level of UHRF2 was higher in the HCC tissues compared with the adjacent non-tumor tissues, but its expression did not exhibit a significant difference between the HepG2 HCC cells and the L02 normal cells. In addition, when comparing the HCC tissues, a higher expression of UHRF2 correlated with a lower expression of H3K9ac in the HCC tissues. The overexpression of UHRF2 increased the expression of H3K9ac in L02 normal cells (P<0.01), but decreased the expression of H3K9ac in HepG2 cancer cells (P<0.05). Moreover, immunofluorescence staining and co-immunoprecipitation assay indicated that UHRF2 co-localized and interacted with H3K9ac in L02 and HepG2 cells and the plant homeodomain (PHD) finger domain was the key domain for UHRF2 directly binding to H3K9ac. Taken together, these results suggest that UHRF2 decreases the expression of H3K9ac in HepG2 HCC cells and interacts with it through the PHD domain.

Indexed as

AcetylationCarcinoma, HepatocellularHep G2 CellsHistonesHumansLiver NeoplasmsLysineProtein BindingProtein DomainsProtein TransportSequence DeletionStructure-Activity RelationshipUbiquitin-Protein LigasesHistonesLysineUbiquitin-Protein LigasesUHRF2 protein, human

Identifiers

PMID28004105
PMCPMC5179198
OpenAlexW2551193893

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.