Evidence map›Paper›PMID 23326372›Full record

ArticlePloS one2013

Mitochondrial telomerase protects cancer cells from nuclear DNA damage and apoptosis.

Chatchawan Singhapol, Deepali Pal, Rafal Czapiewski, Mahendar Porika, Glyn Nelson, Gabriele C Saretzki

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
10.6field-weighted citation impact, top 1% 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

99 citing papers in PubMed, 190 citations in OpenAlex.

  1. Review
  2. Assessing telomerase and Ki-67 protein expression in pre-invasive lesions and invasive cervical neoplasia with correlation to clinico-pathological parameters.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  3. Journal of microbiology and biotechnology · 2026
    Article
  4. Article
  5. Article
  6. Type 2 Diabetes From the Perspective of Telomere Biology.Endocrinology, diabetes & metabolism · 2026
    Review
  7. Review
  8. Telomerase mRNA therapy protects human skin against radiation-induced DNA damage.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Geographic and Viral Etiology Patterns ofInternational journal of molecular sciences · 2025
    Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

39 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

6 authors at 2 institutions in 1 country.

Chatchawan SinghapolInstitute for Ageing and Health, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, United Kingdom.
Deepali Pal
Rafal Czapiewski
Mahendar Porika
Glyn Nelson
Gabriele C Saretzki
Newcastle University · GBNewcastle Hospitals - Campus for Ageing and Vitality · GB

Funding

Biotechnology and Biological Sciences Research Council BB/C008200/1
6 · The paper itself

Abstract

Most cancer cells express high levels of telomerase and proliferate indefinitely. In addition to its telomere maintenance function, telomerase also has a pro-survival function resulting in an increased resistance against DNA damage and decreased apoptosis induction. However, the molecular mechanisms for this protective function remain elusive and it is unclear whether it is connected to telomere maintenance or is rather a non-telomeric function of the telomerase protein, TERT. It was shown recently that the protein subunit of telomerase can shuttle from the nucleus to the mitochondria upon oxidative stress where it protects mitochondrial function and decreases intracellular oxidative stress. Here we show that endogenous telomerase (TERT protein) shuttles from the nucleus into mitochondria upon oxidative stress in cancer cells and analyzed the nuclear exclusion patterns of endogenous telomerase after treatment with hydrogen peroxide in different cell lines. Cell populations excluded TERT from the nucleus upon oxidative stress in a heterogeneous fashion. We found a significant correlation between nuclear localization of telomerase and high DNA damage, while cells which excluded telomerase from the nucleus displayed no or very low DNA damage. We modeled nuclear and mitochondrial telomerase using organelle specific localization vectors and confirmed that mitochondrial localization of telomerase protects the nucleus from inflicted DNA damage and apoptosis while, in contrast, nuclear localization of telomerase correlated with higher amounts of DNA damage and apoptosis. It is known that nuclear DNA damage can be caused by mitochondrially generated reactive oxygen species (ROS). We demonstrate here that mitochondrial localization of telomerase specifically prevents nuclear DNA damage by decreasing levels of mitochondrial ROS. We suggest that this decrease of oxidative stress might be a possible cause for high stress resistance of cancer cells and could be especially important for cancer stem cells.

Indexed as

ApoptosisDNA DamageCell LineCell Line, TumorCell NucleusHeLa CellsHumansHydrogen PeroxideImmunoblottingMCF-7 CellsMicroscopy, ConfocalMitochondriaNeoplasmsOxidantsProtein TransportReactive Oxygen SpeciesHydrogen PeroxideOxidantsReactive Oxygen SpeciesTelomeraseTERT protein, human

Identifiers

PMID23326372
PMCPMC3541395
OpenAlexW2009448733

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.