Evidence map›Paper›PMID 24441046›Full record

ArticleOncogene2015

Dual role of SIRT1 in UVB-induced skin tumorigenesis.

M Ming, K Soltani, C R Shea, X Li, Y Y He

Abstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Trending topics of SIRT1 in tumorigenicity.Biochimica et biophysica acta. General subjects · 2021
    Review
  10. Autophagy of the mNature communications · 2021
    Article
  11. Review
  12. Review
  13. Article
  14. Anti-Wrinkling and Anti-Melanogenic Effect ofInternational journal of molecular sciences · 2019
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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.

M MingSection of Dermatology, Department of Medicine, University of Chicago, Chicago, IL, USA.
K SoltaniSection of Dermatology, Department of Medicine, University of Chicago, Chicago, IL, USA.
C R SheaSection of Dermatology, Department of Medicine, University of Chicago, Chicago, IL, USA.
X LiLaboratory of Signal Transduction, NIEHS, National Institutes of Health, NC, USA.
Y Y HeSection of Dermatology, Department of Medicine, University of Chicago, Chicago, IL, USA.
University of Chicago · US

Funding

VIRAL ONCOLOGY CORE FACILITYP30CA014599 · NCI · UNIVERSITY OF CHICAGO · PI MARK W. LINGEN · 1985 to 2026
$122.1M
TRANSLATIONAL RESEARCH UNIVERSITY OF CHICAGO: CLINICAL TRIALSUL1RR024999 · NCRR · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2007 to 2011
$25.3M
Mechanisms of UVA-induced skin cancerR01ES016936 · NIEHS · UNIVERSITY OF CHICAGO · PI HE, YU-YING · 2010 to 2014
$2.2M
NCI NIH HHS P30 CA014599NCRR NIH HHS UL1 RR024999NCRR NIH HHS UL1RR024999NIEHS NIH HHS ES016936NIEHS NIH HHS R01 ES016936
6 · The paper itself

Abstract

The protein deacetylase SIRT1 regulates various pathways in metabolism, aging and cancer. However, the role of SIRT1 in skin cancer remains unclear. Here, using mice with targeted deletions of SIRT1 in their epidermis in both resistant B6 and sensitive SKH1 hairless backgrounds, we show that the role of SIRT1 in skin cancer development induced by ultraviolet B (UVB) radiation is dependent on its gene dose. Keratinocyte-specific heterozygous deletion of SIRT1 promotes UVB-induced skin tumorigenesis, whereas homozygous deletion of SIRT1 suppresses skin tumor development but sensitizes the B6 mice to chronic solar injury. In mouse skin, SIRT1 is haploinsufficient for UVB-induced DNA damage repair and expression of xeroderma pigmentosum C (XPC), a protein critical for repairing UVB-induced DNA damage. As compared with normal human skin, downregulation of SIRT1 is in parallel with downregulation of XPC in human cutaneous squamous cell carcinoma at both the protein and mRNA levels. In contrast, homozygous SIRT1 deletion in mouse skin augments p53 acetylation and expression of its transcriptional target Noxa, and sensitizes the epidermis to UVB-induced apoptosis in vivo, while heterozygous SIRT1 deletion has no such effect. The gene dosage-dependent function of SIRT1 in DNA repair and cell survival is consistent with the dual roles of SIRT1 in UVB-induced skin tumorigenesis. Our results reveal the gene dosage-dependent in vivo functions of SIRT1 in skin tumorigenesis and may shed light on the role of SIRT1 in epithelial cancer induced by DNA damage.

Indexed as

Ultraviolet RaysAnimalsApoptosisBlotting, WesternCarcinogenesisCell LineDNA-Binding ProteinsDNA DamageDNA RepairFemaleGenotypeHumansMaleMice, Inbred C57BLMice, KnockoutNeoplasms, Radiation-InducedDNA-Binding ProteinsSirt1 protein, mouseSirtuin 1Tumor Suppressor Protein p53Xpc protein, mouse

Identifiers

PMID24441046
PMCPMC4104262
OpenAlexW2056501544

What OpenQuestion holds

Textmetadata
LicenceTDM
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.