Evidence map›Paper›PMID 36699618›Full record

ArticleMolecular therapy oncolytics2023

Zika virus cleaves GSDMD to disseminate prognosticable and controllable oncolysis in a human glioblastoma cell model.

Yu-Ting Kao, Hsin-I Wang, Chi-Ting Shie, Chiou-Feng Lin, Michael M C Lai, Chia-Yi Yu

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy oncolytics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. An Overview of Zika Virus and Zika Virus Induced Neuropathies.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Nanomaterial-induced pyroptosis: a cell type-specific perspective.Frontiers in cell and developmental biology · 2023
    Review
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  17. 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

6 authors at 3 institutions in 1 country.

Yu-Ting KaoNational Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Miaoli 350, Taiwan.
Hsin-I WangNational Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Miaoli 350, Taiwan.
Chi-Ting ShieNational Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Miaoli 350, Taiwan.
Chiou-Feng LinDepartment of Microbiology and Immunology, Taipei Medical University, Taipei 110, Taiwan.
Michael M C LaiResearch Center for Emerging Viruses, China Medical University Hospital, Taichung 404, Taiwan.
Chia-Yi YuNational Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Miaoli 350, Taiwan.
National Health Research Institutes · TWChina Medical University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most common aggressive malignant brain cancer and is chemo- and radioresistant, with poor therapeutic outcomes. The "double-edged sword" of virus-induced cell death could be a potential solution if the oncolytic virus specifically kills cancer cells but spares normal ones. Zika virus (ZIKV) has been defined as a prospective oncolytic virus by selectively targeting GBM cells, but unclear understanding of how ZIKV kills GBM and the consequences hinders its application. Here, we found that the cellular gasdermin D (GSDMD) is required for the efficient death of a human GBM cell line caused by ZIKV infection. The ZIKV protease specifically cleaves human GSDMD to activate caspase-independent pyroptosis, harming both viral protease-harboring and naive neighboring cells. Analyzing human GSDMD variants showed that most people were susceptible to ZIKV-induced cytotoxicity, except for those with variants that resisted ZIKV cleavage or were defective in oligomerizing the N terminus GSDMD cleavage product. Consistently, ZIKV-induced secretion of the pro-inflammatory cytokine interleukin-1β and cytolytic activity were both stopped by a small-molecule inhibitor targeting GSDMD oligomerization. Thus, potential ZIKV oncolytic therapy for GBM would depend on the patient's GSDMD genetic background and could be abolished by GSDMD inhibitors if required.

Indexed as

glioblastoma cellGSDMDoncolysisproteasepyroptosisZika virus

Identifiers

PMID36699618
PMCPMC9845690
OpenAlexW4313529316

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.