Evidence map›Paper›PMID 25893605›Full record

ArticleThe Journal of clinical investigation2015

Telomerase regulates MYC-driven oncogenesis independent of its reverse transcriptase activity.

Cheryl M Koh, Ekta Khattar, Shi Chi Leow, Chia Yi Liu, Julius Muller, Wei Xia Ang, Yinghui Li, Guido Franzoso, Shang Li, Ernesto Guccione and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
9.8field-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

107 citing papers in PubMed, 159 citations in OpenAlex.

  1. Article
  2. Article
  3. Telomerase-Associated Genes as Prognostic Markers in High-Grade Serous Ovarian Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Blocking interplay between TERT and c-Myc: a new therapeutic strategy forInternational journal of biological sciences · 2025
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Telomere Reprogramming and Cellular Metabolism: Is There a Link?International journal of molecular sciences · 2024
    Review
  17. Article
  18. Therapeutic targeting of telomerase ameliorates experimental choroidal neovascularization.Biochimica et biophysica acta. Molecular basis of disease · 2024
    Article
  19. Article
  20. Telomere dysfunction in Tert knockout mice delays BrafInternational journal of cancer · 2024
    Article

47 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

11 authors at 4 institutions in 3 countries.

Cheryl M Koh
Ekta Khattar
Shi Chi Leow
Chia Yi Liu
Julius Muller
Wei Xia Ang
Yinghui Li
Guido Franzoso
Shang Li
Ernesto Guccione
Vinay Tergaonkar
Cancer Genetics (United States) · USNational University of Singapore · SGDuke-NUS Medical School · SGImperial College London · GB

Funding

Cancer Research UK 15115
6 · The paper itself

Abstract

Constitutively active MYC and reactivated telomerase often coexist in cancers. While reactivation of telomerase is thought to be essential for replicative immortality, MYC, in conjunction with cofactors, confers several growth advantages to cancer cells. It is known that the reactivation of TERT, the catalytic subunit of telomerase, is limiting for reconstituting telomerase activity in tumors. However, while reactivation of TERT has been functionally linked to the acquisition of several "hallmarks of cancer" in tumors, the molecular mechanisms by which this occurs and whether these mechanisms are distinct from the role of telomerase on telomeres is not clear. Here, we demonstrated that first-generation TERT-null mice, unlike Terc-null mice, show delayed onset of MYC-induced lymphomagenesis. We further determined that TERT is a regulator of MYC stability in cancer. TERT stabilized MYC levels on chromatin, contributing to either activation or repression of its target genes. TERT regulated MYC ubiquitination and proteasomal degradation, and this effect of TERT was independent of its reverse transcriptase activity and role in telomere elongation. Based on these data, we conclude that reactivation of TERT, a direct transcriptional MYC target in tumors, provides a feed-forward mechanism to potentiate MYC-dependent oncogenesis.

Indexed as

AnimalsCell Line, TumorCell Transformation, NeoplasticEnzyme ActivationFeedback, PhysiologicalGene Expression Regulation, NeoplasticGenes, mycGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHeterograftsHumansLymphoma, Non-HodgkinMiceMice, Inbred C57BLMice, KnockoutNeoplasm ProteinsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaMyc protein, mouseNeoplasm ProteinsProto-Oncogene Proteins c-mycRNATelomerasetelomerase RNATert protein, mouse

Identifiers

PMID25893605
PMCPMC4463203
OpenAlexW2112891249

What OpenQuestion holds

Textmetadata
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.