Evidence map›Paper›PMID 24156782›Full record

ArticleMolecular cancer2013

A novel Hsp90 inhibitor AT13387 induces senescence in EBV-positive nasopharyngeal carcinoma cells and suppresses tumor formation.

King Chi Chan, Choi Man Ting, Pui Shan Chan, Ming Chu Lo, Kwok Wai Lo, Jayne E Curry, Tomoko Smyth, Anne Wing Mui Lee, Wai Tong Ng, George Sai Wah Tsao and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.1field-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

36 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. HDAC6-mediated deacetylation of FLOT2 maintains stability and tumorigenic function of FLOT2 in nasopharyngeal carcinoma.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Signaling pathways of EBV-induced oncogenesis.Cancer cell international · 2021
    Review
  15. The Paradoxical Role of Cellular Senescence in Cancer.Frontiers in cell and developmental biology · 2021
    Review
  16. Article
  17. Review
  18. Review
  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

13 authors at 4 institutions in 2 countries.

King Chi Chan
Choi Man Ting
Pui Shan Chan
Ming Chu Lo
Kwok Wai Lo
Jayne E Curry
Tomoko Smyth
Anne Wing Mui Lee
Wai Tong Ng
George Sai Wah Tsao
Ricky Ngok Shun Wong
Maria Li Lung
Nai Ki MakDepartment of Biology, Hong Kong Baptist University, Hong Kong, P,R, China. nkmak@hkbu.edu.hk.
Hong Kong Baptist University · HKUniversity of Hong Kong · HKChinese University of Hong Kong · CNPamela Youde Nethersole Eastern Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNasopharyngeal carcinoma (NPC) is an epithelial malignancy strongly associated with Epstein-Barr virus (EBV). AT13387 is a novel heat shock protein 90 (Hsp90) inhibitor, which inhibits the chaperone function of Hsp90 and reduces expression of Hsp90-dependent client oncoproteins. This study aimed to evaluate both the in vitro and in vivo antitumor effects of AT13387 in the EBV-positive NPC cell line C666-1.

resultsOur results showed that AT13387 inhibited C666-1 cell growth and induced cellular senescence with the downregulation of multiple Hsp90 client oncoproteins EGFR, AKT, CDK4, and restored the protein expression of negative cell cycle regulator p27. We also studied the ability of AT13387 to restore p27 expression by downregulation of AKT and the p27 ubiquitin mediator, Skp2, using AKT inhibitor and Skp2 siRNA. In the functional study, AT13387 inhibited cell migration with downregulation of a cell migration regulator, HDAC6, and increased the acetylation and stabilization of α-tubulin. We also examined the effect of AT13387 on putative cancer stem cells (CSC) by 3-D tumor sphere formation assay. AT13387 effectively reduced both the number and size of C666-1 tumor spheres with decreased expression of NPC CSC-like markers CD44 and SOX2. In the in vivo study, AT13387 significantly suppressed tumor formation in C666-1 NPC xenografts.

conclusionAT13387 suppressed cell growth, cell migration, tumor sphere formation and induced cellular senescence on EBV-positive NPC cell line C666-1. Also, the antitumor effect of AT13387 was demonstrated in an in vivo model. This study provided experimental evidence for the preclinical value of using AT13387 as an effective antitumor agent in treatment of NPC.

Indexed as

AcetylationAnimalsAntineoplastic AgentsBenzamidesCarcinomaCell Line, TumorCell ProliferationCell SurvivalCellular SenescenceEpstein-Barr Virus InfectionsFemaleHistone Deacetylase 6Histone DeacetylasesHSP90 Heat-Shock ProteinsHumansHyaluronan Receptors(2,4-dihydroxy-5-isopropylphenyl)-(5-(4-methylpiperazin-1-ylmethyl)-1,3-dihydroisoindol-2-yl)methanoneAntineoplastic AgentsBenzamidesCD44 protein, humanHDAC6 protein, humanHistone Deacetylase 6Histone DeacetylasesHSP90 Heat-Shock ProteinsHyaluronan ReceptorsIsoindolesSOX2 protein, humanSOXB1 Transcription FactorsTubulin

Identifiers

PMID24156782
PMCPMC3834878
OpenAlexW2131697316

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.