Evidence map›Paper›PMID 31963842›Full record

ArticleInternational journal of molecular sciences2020

CRISPR/Cas9-Mediated TERT Disruption in Cancer Cells.

Luan Wen, Changzhi Zhao, Jun Song, Linyuan Ma, Jinxue Ruan, Xiaofeng Xia, Y Eugene Chen, Jifeng Zhang, Peter X Ma, Jie Xu

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Crosstalk BetweenCancers · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Role of Telomeres and Telomerase in Cancer and Aging.International journal of molecular sciences · 2023
    Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  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

10 authors at 1 institution in 1 country.

Luan WenCenter for Advanced Models and Translational Sciences and Therapeutics, University of Michigan, Ann Arbor, MI 48109, USA.
Changzhi ZhaoCenter for Advanced Models and Translational Sciences and Therapeutics, University of Michigan, Ann Arbor, MI 48109, USA.
Jun SongCenter for Advanced Models and Translational Sciences and Therapeutics, University of Michigan, Ann Arbor, MI 48109, USA.ORCID 0000-0002-6128-6378
Linyuan MaCenter for Advanced Models and Translational Sciences and Therapeutics, University of Michigan, Ann Arbor, MI 48109, USA.
Jinxue RuanCenter for Advanced Models and Translational Sciences and Therapeutics, University of Michigan, Ann Arbor, MI 48109, USA.
Xiaofeng XiaResearch & Development, ATGC Inc. 100 E Lancaster Avenue, LIMR Building Lab129, Wynnewood, PA 19096, USA.
Y Eugene ChenCenter for Advanced Models and Translational Sciences and Therapeutics, University of Michigan, Ann Arbor, MI 48109, USA.
Jifeng ZhangCenter for Advanced Models and Translational Sciences and Therapeutics, University of Michigan, Ann Arbor, MI 48109, USA.
Peter X MaDepartment of Biologic and Materials Sciences, University of Michigan, Ann Arbor, MI 48109, USA.ORCID 0000-0002-0191-9487
Jie XuCenter for Advanced Models and Translational Sciences and Therapeutics, University of Michigan, Ann Arbor, MI 48109, USA.
University of Michigan · US

Funding

A nanoparticle delivery system for CRISPR/Cas9 based therapeuticsR42TR001711 · NCATS · ATGC, INC. · PI KURODA, KENICHI · 2017 to 2019
$1.7M
NCATS NIH HHS R42 TR001711NIH HHS AG055863NIH HHS TR001711
6 · The paper itself

Abstract

Mammalian telomere lengths are primarily regulated by telomerase, a ribonucleoprotein consisting of a reverse transcriptase (TERT) and an RNA subunit (TERC). TERC is constitutively expressed in all cells, whereas TERT expression is temporally and spatially regulated, such that in most adult somatic cells, TERT is inactivated and telomerase activity is undetectable. Most tumor cells activate TERT as a mechanism for preventing progressive telomere attrition to achieve proliferative immortality. Therefore, inactivating TERT has been considered to be a promising means of cancer therapy. Here we applied the CRISPR/Cas9 gene editing system to target the TERT gene in cancer cells. We report that disruption of TERT severely compromises cancer cell survival in vitro and in vivo. Haploinsufficiency of TERT in tumor cells is sufficient to result in telomere attrition and growth retardation in vitro. In vivo, TERT haploinsufficient tumor cells failed to form xenograft after transplantation to nude mice. Our work demonstrates that gene editing-mediated TERT knockout is a potential therapeutic option for treating cancer.

Indexed as

AnimalsCell Line, TumorCell ProliferationCell SurvivalCRISPR-Cas SystemsFemaleGene Knockout TechniquesHaploinsufficiencyHeLa CellsHumansINDEL MutationMiceMice, NudeNeoplasm TransplantationTelomeraseUterine Cervical NeoplasmsTelomeraseTERT protein, humancancer therapyCRISPR/Cas9gene editingtelomeraseTERT

Identifiers

PMID31963842
PMCPMC7014288
OpenAlexW2999841812

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.