Evidence map›Paper›PMID 30696954›Full record

ArticleOncogene2019

Cancer therapy with a CRISPR-assisted telomerase-activating gene expression system.

Wei Dai, Xinhui Xu, Danyang Wang, Jian Wu, Jinke Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Designing nucleic acid-based therapeutics for cancer treatment: Updates on the state of the art.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. CRISPR-based mFrontiers in cell and developmental biology · 2023
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Targeting Cancer with CRISPR/Cas9-Based Therapy.International journal of molecular sciences · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Dead Cas Systems: Types, Principles, and Applications.International journal of molecular sciences · 2019
    Review
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.

Wei DaiState Key Laboratory of Bioelectronics, Southeast University, 210096, Nanjing, China.
Xinhui XuState Key Laboratory of Bioelectronics, Southeast University, 210096, Nanjing, China.
Danyang WangState Key Laboratory of Bioelectronics, Southeast University, 210096, Nanjing, China.
Jian WuState Key Laboratory of Bioelectronics, Southeast University, 210096, Nanjing, China.
Jinke WangState Key Laboratory of Bioelectronics, Southeast University, 210096, Nanjing, China. wangjinke@seu.edu.cn.ORCID http://orcid.org/0000-0002-3352-4690
Southeast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is caused by a series of alterations in genome and epigenome and exists in multiple complex forms, making it difficult to be prevented and/or treated. Telomerase, an enzyme responsible for the maintenance of telomere, is silent in most normal somatic cells but activated in 90% of cancer cells, making it an excellent target for cancer therapy. Therefore, various telomerase activity inhibitors have been developed to treat cancer but all failed due to side effects. Here we acted oppositely to develop a cancer gene therapy named telomerase-activating gene expression (Tage) system by utilizing the telomerase activity in cancer cells. The Tage system consisted of an effector gene expression vector that carried a 3' telomerase-recognizable stick end and an artificial transcription factor expression vector that could express dCas9-VP64 and an sgRNA targeting telomere repeat sequences. By using Cas9 as an effector gene, the Tage system effectively killed various cancer cells, including HepG2, HeLa, PANC-1, MDA-MB-453, A549, HT-29, SKOV-3, Hepa1-6, and RAW264.7, without affecting normal cells MRC-5, HL7702, and bone marrow mesenchymal stem cell (BMSC). More importantly, a four-base 3' stick end produced by the homothallic switching endonuclease in cells could be recognized by telomerase, allowing the Tage system to effectively kill cancer cells in vivo. The Tage system could effectively and safely realize its in vivo application by using adeno-associated virus (AAV) as gene vector. The virus-loaded Tage system could significantly and specifically kill cancer cells in mice by intravenous drug administration without side effects or toxicity.

Indexed as

AnimalsCell LineCell Line, TumorClustered Regularly Interspaced Short Palindromic RepeatsDependovirusGene ExpressionGene Expression RegulationGenetic TherapyGenetic VectorsHEK293 CellsHeLa CellsHep G2 CellsHumansMesenchymal Stem CellsMiceNeoplasmsTelomerase

Identifiers

PMID30696954
OpenAlexW2951800859

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.