Evidence map›Paper›PMID 23800953›Full record

ArticleOncotarget2013

Mechanism of DNA damage responses induced by exposure to an oligonucleotide homologous to the telomere overhang in melanoma.

Ryan T Pitman, Luke Wojdyla, Neelu Puri

Open access · hybridAbstract read
In one paragraph

Article in Oncotarget, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
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  9. Treating Cancer by Targeting Telomeres and Telomerase.Antioxidants (Basel, Switzerland) · 2017
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. T-oligo as an anticancer agent in colorectal cancer.Biochemical and biophysical research communications · 2014
    Article
  18. Article
  19. Article
  20. Beyond Telomerase: Telomere Instability as a Novel Target for Cancer Therapy.Journal of molecular and genetic medicine : an international journal of biomedical research · 2013
    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

3 authors at 1 institution in 1 country.

Ryan T PitmanDepartment of Biomedical Sciences, University of Illinois College of Medicine, Rockford, Illinois, USA.
Luke Wojdyla
Neelu Puri
Illinois College · US

Funding

The Effect of the Telomere 3'Overhang DNA on Melanoma.R03AR050110 · NIAMS · UNIVERSITY OF CHICAGO · PI PURI, NEELU · 2003 to 2005
$229k
NIAMS NIH HHS 7R03AR050110NIAMS NIH HHS R03 AR050110
6 · The paper itself

Abstract

T-oligo, an 11-base oligonucleotide homologous to the 3'-telomeric overhang, is a novel, potent therapeutic modality in melanoma and multiple other tumor types. T-oligo is proposed to function in a manner similar to experimental disruption of the telomere overhang and induces DNA damage responses including apoptosis, differentiation and senescence. However, important components involved in T-oligo induced responses are not defined, particularly the role of p53, TRF1 and TRF2 in mediating the T-oligo induced responses. In MU, PM-WK, and MM-MC melanoma cells, exposure to T-oligo upregulates p53 expression and phosphorylation, resulting in cellular differentiation and activation of a caspase-mediated apoptotic cascade. However, siRNA-mediated knockdown of p53 completely blocks T-oligo induced differentiation and significantly decreases apoptosis, suggesting that p53 is an important mediator of T-oligo induced responses. In addition, we characterized the roles of telomere binding proteins, TRF1, TRF2, and tankyrase-1, in T-oligo induced damage responses. We demonstrate that tankyrase-1 activity is required for initiation of T-oligo induced damage responses including p53 phosphorylation and reduction of cellular proliferation. These results highlight TRF1, TRF2, tankyrase-1 and p53 as important elements in T-oligo mediated responses and suggest new avenues for research into T-oligo's mechanism of action.

Indexed as

ApoptosisCell DifferentiationCell Line, TumorCell ProliferationCellular SenescenceDNA DamageDNA RepairGene ExpressionHeterocyclic Compounds, 3-RingHumansMelanomaOligonucleotidesPhosphorylationRNA InterferenceRNA, Small InterferingSkin NeoplasmsHeterocyclic Compounds, 3-RingOligonucleotidesRNA, Small InterferingTankyrasesTelomeric Repeat Binding Protein 1Telomeric Repeat Binding Protein 2TNKS protein, humanTumor Suppressor Protein p53XAV939

Identifiers

PMID23800953
PMCPMC3742836
OpenAlexW1564838069

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.