Evidence map›Paper›PMID 27824900›Full record

ArticlePloS one2016

SIRT6 Depletion Suppresses Tumor Growth by Promoting Cellular Senescence Induced by DNA Damage in HCC.

Namgyu Lee, Hye Guk Ryu, Jung-Hee Kwon, Dae-Kyum Kim, Sae Rom Kim, Hee Jung Wang, Kyong-Tai Kim, Kwan Yong Choi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  7. Review
  8. The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Emerging Therapeutic Potential of SIRT6 Modulators.Journal of medicinal chemistry · 2021
    Review
  16. Article
  17. Review
  18. Review
  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

8 authors at 3 institutions in 2 countries.

Namgyu LeeDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk, Korea.
Hye Guk RyuDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk, Korea.
Jung-Hee KwonCbs Bioscience Inc., Daejeon, Korea.
Dae-Kyum KimDonnelly Centre, Departments of Molecular Genetics and Computer Science, University of Toronto, Toronto, Ontario, Canada.
Sae Rom KimDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk, Korea.
Hee Jung WangDepartment of Surgery, Ajou University School of Medicine, Suwon, Korea.
Kyong-Tai KimDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk, Korea.
Kwan Yong ChoiDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk, Korea.
Pohang University of Science and Technology · KRAjou University · KRMount Sinai Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of Sirtuin 6 (SIRT6) as a tumor suppressor or oncogene in liver cancer remains controversial. Thus, we identified the specific role of SIRT6 in the progression of hepatocellular carcinoma (HCC). SIRT6 expression was significantly higher in HCC cell lines and HCC tissues from 138 patients than in an immortalized hepatocyte cell line, THLE-2 and non-tumor tissues, respectively. SIRT6 knockdown by shRNA suppressed the growth of HCC cells and inhibited HCC tumor growth in vivo. In addition, SIRT6 silencing significantly prevented the growth of HCC cell lines by inducing cellular senescence in the p16/Rb- and p53/p21-pathway independent manners. Microarray analysis revealed that the expression of genes involved in nucleosome assembly was apparently altered in SIRT6-depleted Hep3B cells. SIRT6 knockdown promoted G2/M phase arrest and downregulation of genes encoding histone variants associated with nucleosome assembly, which could be attributed to DNA damage. Taken together, our findings suggest that SIRT6 acts as a tumor promoter by preventing DNA damage and cellular senescence, indicating that SIRT6 represents a potential therapeutic target for the treatment of HCC.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorCellular SenescenceDNA DamageGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLiver NeoplasmsMaleMiceMice, NudeNeoplasm TransplantationOligonucleotide Array Sequence AnalysisSirtuinsSIRT6 protein, humanSirtuins

Identifiers

PMID27824900
PMCPMC5100879
OpenAlexW2555013871

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.