Evidence map›Paper›PMID 31637166›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2019

The CRISPR-Cas13a Gene-Editing System Induces Collateral Cleavage of RNA in Glioma Cells.

Qixue Wang, Xing Liu, Junhu Zhou, Chao Yang, Guangxiu Wang, Yanli Tan, Ye Wu, Sijing Zhang, Kaikai Yi, Chunsheng Kang

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

88 citing papers in PubMed, 181 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Programmable RNA NAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. A Chemically Induced CRISPR/dCas13Journal of medicinal chemistry · 2025
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Precise progerin targeting using RfxCas13d: A therapeutic avenue for Hutchinson-Gilford progeria syndrome.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  20. Article

28 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

10 authors at 3 institutions in 1 country.

Qixue WangTianjin Medical University General Hospital Tianjin Neurological Institute Key Laboratory of Post-neurotrauma Neuro-repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Department of Neurosurgery Tianjin Medical University General Hospital Tianjin 300052 China.
Xing LiuBeijing Neurosurgical Institute Capital Medical University Beijing 100050 China.
Junhu ZhouTianjin Medical University General Hospital Tianjin Neurological Institute Key Laboratory of Post-neurotrauma Neuro-repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Department of Neurosurgery Tianjin Medical University General Hospital Tianjin 300052 China.
Chao YangTianjin Medical University General Hospital Tianjin Neurological Institute Key Laboratory of Post-neurotrauma Neuro-repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Department of Neurosurgery Tianjin Medical University General Hospital Tianjin 300052 China.
Guangxiu WangTianjin Medical University General Hospital Tianjin Neurological Institute Key Laboratory of Post-neurotrauma Neuro-repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Department of Neurosurgery Tianjin Medical University General Hospital Tianjin 300052 China.
Yanli TanDepartment of Pathology Medical College of Hebei University Baoding Hebei 071000 China.
Ye WuTianjin Medical University General Hospital Tianjin Neurological Institute Key Laboratory of Post-neurotrauma Neuro-repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Department of Neurosurgery Tianjin Medical University General Hospital Tianjin 300052 China.
Sijing ZhangTianjin Medical University General Hospital Tianjin Neurological Institute Key Laboratory of Post-neurotrauma Neuro-repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Department of Neurosurgery Tianjin Medical University General Hospital Tianjin 300052 China.
Kaikai YiTianjin Medical University General Hospital Tianjin Neurological Institute Key Laboratory of Post-neurotrauma Neuro-repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Department of Neurosurgery Tianjin Medical University General Hospital Tianjin 300052 China.
Chunsheng KangTianjin Medical University General Hospital Tianjin Neurological Institute Key Laboratory of Post-neurotrauma Neuro-repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Department of Neurosurgery Tianjin Medical University General Hospital Tianjin 300052 China.ORCID https://orcid.org/0000-0002-3255-3369
Tianjin Medical University General Hospital · CNCapital Medical University · CNHebei University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RNA is rarely used as a therapeutic target due to its flexible structure and instability. CRISPR-Cas13a is a powerful tool for RNA knockdown, and the potential application of CRISPR-Cas13a in cancer cells should be further studied. In this study, overexpression of LwCas13a by lentivirus in glioma cells reveals that crRNA-EGFP induces a "collateral effect" after knocking down the target gene in EGFP-expressing cells. EGFRvIII is a unique EGFR mutant subtype in glioma, and the CRISPR-Cas13a system induces death in EGFRvIII-overexpressing glioma cells. Bulk and single-cell RNA sequencing analysis in U87-Cas13a-EGFRvIII cells confirm the collateral effect of the CRISPR-Cas13a system. Furthermore, CRISPR-Cas13a inhibits the formation of glioma intracranial tumors in mice. The results demonstrate the collateral effect of the CRISPR-Cas13a system in cancer cells and the powerful tumor-eliminating potential of this system.

Indexed as

collateral effectCRISPR‐Cas13aEGFRvIIIglioblastoma (GBM)

Identifiers

PMID31637166
PMCPMC6794629
OpenAlexW2970054604

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.