Evidence map›Paper›PMID 25880358›Full record

ArticleScientific reports2015

Enhancer of rudimentary homolog regulates DNA damage response in hepatocellular carcinoma.

Meng-Tzu Weng, Tzu-Hsun Tung, Jih-Hsiang Lee, Shu-Chen Wei, Hang-Li Lin, Yu-Jung Huang, Jau-Min Wong, Ji Luo, Jin-Chuan Sheu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. ERH Impacts Patient Prognosis and Tumor Immune Microenvironment: A Pan-Cancer Analysis.Combinatorial chemistry & high throughput screening · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. ERH Gene and Its Role in Cancer Cells.Frontiers in oncology · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
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  19. Review
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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

9 authors at 3 institutions in 2 countries.

Meng-Tzu Weng1] Graduate Institute of Clinical Medicine, National Taiwan University, Taipei 100, Taiwan [2] Far-Eastern Memorial Hospital, New Taipei 220, Taiwan.
Tzu-Hsun TungLiver Disease Prevention and Treatment Research Foundation, Taipei 100, Taiwan.
Jih-Hsiang LeeClinical Trial Center, Taipei 100, Taiwan.
Shu-Chen WeiDepartment of Internal Medicine, National Taiwan University Hospital and College of Medicine, Taipei 100, Taiwan.
Hang-Li LinDepartment of Internal Medicine, National Taiwan University Hospital and College of Medicine, Taipei 100, Taiwan.
Yu-Jung HuangLiver Disease Prevention and Treatment Research Foundation, Taipei 100, Taiwan.
Jau-Min WongDepartment of Internal Medicine, National Taiwan University Hospital and College of Medicine, Taipei 100, Taiwan.
Ji LuoCancer Systems Biology Section, Laboratory of Cancer Biology and Genetics, National Cancer Institute, NIH Bethesda, MD 20892, USA.
Jin-Chuan SheuDepartment of Internal Medicine, National Taiwan University Hospital and College of Medicine, Taipei 100, Taiwan.
National Taiwan University Hospital · TWNational Cancer Institute · USNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously demonstrated that the enhancer of rudimentary homolog (ERH) gene is required for the expression of multiple cell cycle and DNA damage response (DDR) genes. The present study investigated the role of ERH and its target DNA damage repair genes in hepatocellular carcinoma cells. We observed positive correlation between ERH and ataxia telangiectasia and Rad3 related (ATR) expression in liver tissues. Expression of ERH, ATR as well as checkpoint kinase 1 (CHK1) were higher in HCCs than in normal liver tissues. Knocking-down ERH augmented ultraviolet light induced DNA damage in HepG2 cells. ATR protein level is reduced upon ERH depletion as a result of defect in the splicing of ATR mRNA. Consequently, the ATR effector kinase Chk1 failed to be phosphorylated upon ultraviolet light or hydroxyurea treatment in ERH knocked-down HepG2 cells. Finally, we observed Chk1 inhibitor AZD7762 enhanced the effect of doxorubicin on inhibiting growth of HCC cells in vitro and in vivo. This study suggested that ERH regulates the splicing of the DNA damage response proteins ATR in HCC cells, and targeting DNA damage response by Chk1 inhibitor augments chemotherapy to treat HCC cells.

Indexed as

DNA DamageDNA RepairAnimalsAntibiotics, AntineoplasticAtaxia Telangiectasia Mutated ProteinsCarcinoma, HepatocellularCell Cycle ProteinsCell ProliferationCheckpoint Kinase 1Drug SynergismHep G2 CellsHumansLiverLiver NeoplasmsMaleMiceAntibiotics, AntineoplasticAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCheckpoint Kinase 1CHEK1 protein, humanChek1 protein, mouseERH protein, humanProtein KinasesRNA, MessengerTranscription Factors

Identifiers

PMID25880358
PMCPMC4399501
OpenAlexW2042109342

What OpenQuestion holds

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LicenceCC BY
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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.