Evidence map›Paper›PMID 21472714›Full record

ArticleCancer2011

Sirtuin-3 (SIRT3), a novel potential therapeutic target for oral cancer.

Turki Y Alhazzazi, Pachiyappan Kamarajan, Nam Joo, Jing-Yi Huang, Eric Verdin, Nisha J D'Silva, Yvonne L Kapila

Open access · bronzeAbstract read
In one paragraph

Article in Cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 4% 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

110 citing papers in PubMed, 1 synthesis or guideline pooled it, 217 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. NADAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

50 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Turki Y AlhazzaziDepartment of Periodontics and Oral Medicine, School of Dentistry, University of Michigan, Ann Arbor, Michigan 48109-1078, USA.
Pachiyappan Kamarajan
Nam Joo
Jing-Yi Huang
Eric Verdin
Nisha J D'Silva
Yvonne L Kapila
University of Michigan · USGladstone Institutes · US

Funding

FIBRONECTIN REGULATION OF CARCINOMA APOPTOSISR01DE014429 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAPILA, YVONNE L · 2004 to 2009
$1.3M
Fibronectin Regulation of AnoikisR56DE014429 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAPILA, YVONNE L · 2010 to 2010
$367k
NIDCR NIH HHS R01 DE014429NIDCR NIH HHS R56 DE014429PHS HHS R01 DEO14429
6 · The paper itself

Abstract

backgroundSeveral sirtuin family members (SIRT1-7), which are evolutionarily conserved NAD-dependent deacetylases, play an important role in carcinogenesis. However, their role in oral cancer has not yet been investigated. Therefore, the objective of this study was to investigate whether sirtuins play a role in oral cancer carcinogenesis.

methodsThe expression levels of all sirtuins in several oral squamous cell carcinoma (OSCC) cell lines were compared with normal human oral keratinocytes and observed that SIRT3 was highly expressed. Therefore, tissue microarrays were used to evaluate the clinical relevance of this overexpression. SIRT3 down-regulation in OSCC cell proliferation and survival was investigated and analyzed by using cell-proliferation and cell-viability assays. Ionizing radiation and cisplatin were used to investigate whether SIRT3 down-regulation could increase the sensitivity of OSCC to both treatments. To further assess the in vivo role of SIRT3 in OSCC carcinogenesis, a floor-of-mouth oral cancer murine model was used to study the effect of SIRT3 down-regulation on OSCC tumor growth in immunodeficient mice.

resultsThe current results demonstrated for the first time that SIRT3 is overexpressed in OSCC in vitro and in vivo compared with other sirtuins. Down-regulation of SIRT3 inhibited OSCC cell growth and proliferation and increased OSCC cell sensitivity to radiation and cisplatin treatments in vitro. SIRT3 down-regulation also reduced tumor burden in vivo.

conclusionsThe current investigation revealed a novel role for SIRT3 in oral cancer carcinogenesis as a promoter of cell proliferation and survival, thus implicating SIRT3 as a new potential therapeutic target to treat oral cancer.

Indexed as

AnimalsCarcinoma, Squamous CellCell Line, TumorCell ProliferationCell SurvivalHumansMiceMice, NudeMolecular Targeted TherapyMouth NeoplasmsRadiation ToleranceSirtuin 3Up-RegulationSirtuin 3

Identifiers

PMID21472714
PMCPMC3117020
OpenAlexW2068289009

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.