Evidence map›Paper›PMID 24370995›Full record

ArticleApoptosis : an international journal on programmed cell death2014

Induction of autophagy-dependent cell death by the survivin suppressant YM155 in salivary adenoid cystic carcinoma.

Yu-Fan Wang, Wei Zhang, Ke-Fei He, Bing Liu, Lu Zhang, Wen-Feng Zhang, Ashok B Kulkarni, Yi-Fang Zhao, Zhi-Jun Sun

Abstract read
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Article
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  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Frontiers in oncology · 2019
    Article
  11. Article
  12. Article
  13. YM155 Down-Regulates Survivin and Induces P53 Up-Regulated Modulator of Apoptosis (PUMA)-Dependent in Oral Squamous Cell Carcinoma Cells.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  14. Article
  15. Silencing Livin induces apoptotic and autophagic cell death, increasing chemotherapeutic sensitivity to cisplatin of renal carcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. Article
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  19. Inhibition of Survivin with YM155 Induces Durable Tumor Response in Anaplastic Thyroid Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015
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  20. 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

9 authors at 2 institutions in 2 countries.

Yu-Fan WangThe State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, Department of Oral and Maxillofacial-Head and Neck Oncology, School and Hospital of Stomatology, Wuhan University, Wuhan, 430079, China.
Wei Zhang
Ke-Fei He
Bing Liu
Lu Zhang
Wen-Feng Zhang
Ashok B Kulkarni
Yi-Fang Zhao
Zhi-Jun Sun
Wuhan University · CNNational Institutes of Health · US

Funding

Molecular Roles of Cdk5 in Neuronal Functions and Pain SignalingZIADE000664 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI KULKARNI, ASHOK · 2009 to 2025
$20.4M
Molecular Roles of TGF-beta Signaling in Salivary Glands and Oral CancerZIADE000723 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI KULKARNI, ASHOK · 2009 to 2012
$2.4M
Intramural NIH HHS ZIA DE000723
6 · The paper itself

Abstract

Adenoid cystic carcinoma (ACC) is one of the most common malignancies of the major and minor salivary glands. However, the molecular mechanism underlying the aggressive growth of human salivary ACC remains unclear. In the present study, we showed that survivin, which belongs to the family of inhibitors of apoptosis, is closely related to the high expression of CDK4 and cyclin D1 in human ACC specimens. By employing the small-molecule drug YM155, we found that the inhibition of survivin in ACC cells caused significant cell death and induced autophagy. Chloroquine, an autophagy inhibitor, prevented cell death induced by YM155, suggesting YM155-induced autophagy contributed to the cell death effects in ACC cells. More importantly, evidence obtained from a xenograft model using ACC-2 cells proved the occurrence of YM155-induced autophagy and cell death in vivo was correlated with the suppression of Erk1/2 and S6 activation as well as increased TFEB nuclear translocation. Taken together, our results indicate YM155 is a novel inducer of autophagy-dependent cell death and possesses therapeutic potential in ACC.

Indexed as

AnimalsAntineoplastic AgentsApoptosisAutophagyCarcinoma, Adenoid CysticCell Line, TumorFemaleHeterograftsHumansImidazolesInhibitor of Apoptosis ProteinsMiceMice, Inbred BALB CMice, NudeMouth NeoplasmsNaphthoquinonesAntineoplastic AgentsBIRC5 protein, humanImidazolesInhibitor of Apoptosis ProteinsNaphthoquinonessepantroniumSurvivin

Identifiers

PMID24370995
PMCPMC4211076
OpenAlexW2068305806

What OpenQuestion holds

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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.