Evidence map›Paper›PMID 28607091›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Selective replication of oncolytic virus M1 results in a bystander killing effect that is potentiated by Smac mimetics.

Jing Cai, Yuan Lin, Haipeng Zhang, Jiankai Liang, Yaqian Tan, Webster K Cavenee, Guangmei Yan

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Oncolytic virus M1 reinvigorates CD8Cellular & molecular immunology · 2026
    Article
  6. Identification of TPRA1 as a Novel Receptor and Predictive Biomarker for Oncolytic Virus M1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  7. TAMs-mediated resistance to oncolytic virus M1 in solid tumors.Journal for immunotherapy of cancer · 2025
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. cIAP1/2 Antagonism Induces Antigen-Specific T Cell-Dependent Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  17. Review
  18. Overcoming resistance to oncolytic virus M1 by targeting PI3K-γ in tumor-associated myeloid cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  19. Article
  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

7 authors at 2 institutions in 2 countries.

Jing CaiDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China.
Yuan LinDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China.
Haipeng ZhangDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China.
Jiankai LiangDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China.
Yaqian TanDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China.
Webster K CaveneeLudwig Institute for Cancer Research, University of California, San Diego, CA 92093-0660 wcavenee@ucsd.edu ygm@mail.sysu.edu.cn.ORCID 0000-0003-3804-9179
Guangmei YanDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; wcavenee@ucsd.edu ygm@mail.sysu.edu.cn.
Sun Yat-sen University · CNUniversity of California San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncolytic virotherapy is a treatment modality that uses native or genetically modified viruses that selectively replicate in and kill tumor cells. Viruses represent a type of pathogen-associated molecular pattern and thereby induce the up-regulation of dozens of cytokines via activating the host innate immune system. Second mitochondria-derived activator of caspases (Smac) mimetic compounds (SMCs), which antagonize the function of inhibitor of apoptosis proteins (IAPs) and induce apoptosis, sensitize tumor cells to multiple cytokines. Therefore, we sought to determine whether SMCs sensitize tumor cells to cytokines induced by the oncolytic M1 virus, thus enhancing a bystander killing effect. Here, we report that SMCs potentiate the oncolytic effect of M1 in vitro, in vivo, and ex vivo. This strengthened oncolytic efficacy resulted from the enhanced bystander killing effect caused by the M1 virus via cytokine induction. Through a microarray analysis and subsequent validation using recombinant cytokines, we identified IL-8, IL-1A, and TRAIL as the key cytokines in the bystander killing effect. Furthermore, SMCs increased the replication of M1, and the accumulation of virus protein induced irreversible endoplasmic reticulum stress- and c-Jun N-terminal kinase-mediated apoptosis. Nevertheless, the combined treatment with M1 and SMCs had little effect on normal and human primary cells. Because SMCs selectively and significantly enhance the bystander killing effect and the replication of oncolytic virus M1 specifically in cancer cells, this combined treatment may represent a promising therapeutic strategy.

Indexed as

AnimalsApoptosisBystander EffectCell Line, TumorCytokinesHumansMiceNeoplasms, ExperimentalOligopeptidesOncolytic VirusesPeptidomimeticsVirus ReplicationCytokinesOligopeptidesPeptidomimeticsSMAC peptidebystander killing effectoncolytic virusSMAC mimetics

Identifiers

PMID28607091
PMCPMC5495246
OpenAlexW2626668730

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.