Evidence map›Paper›PMID 26252575›Full record

ArticleOncology reports2015

Nutlin-3 sensitizes nasopharyngeal carcinoma cells to cisplatin-induced cytotoxicity.

Yee-Lin Voon, Munirah Ahmad, Pooi-Fong Wong, Roslina Husaini, Wayne Tiong-Weng Ng, Chee-Onn Leong, David Philip Lane, Alan Soo-Beng Khoo

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 39 citations in OpenAlex.

  1. Role of the MDM2/p53 axis in regulating cisplatin response in tumor cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. E3 ubiquitin ligases in nasopharyngeal carcinoma and implications for therapies.Journal of molecular medicine (Berlin, Germany) · 2023
    Article
  6. Review
  7. Article
  8. Review
  9. Therapeutics Targeting p53-MDM2 Interaction to Induce Cancer Cell Death.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. An evaluationOncotarget · 2018
    Article
  19. Review
  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

8 authors at 4 institutions in 2 countries.

Yee-Lin VoonMolecular Pathology Unit, Cancer Research Centre, Institute for Medical Research, Kuala Lumpur 50588, Malaysia.
Munirah AhmadMolecular Pathology Unit, Cancer Research Centre, Institute for Medical Research, Kuala Lumpur 50588, Malaysia.
Pooi-Fong WongDepartment of Pharmacology, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia.
Roslina HusainiMolecular Pathology Unit, Cancer Research Centre, Institute for Medical Research, Kuala Lumpur 50588, Malaysia.
Wayne Tiong-Weng NgMolecular Pathology Unit, Cancer Research Centre, Institute for Medical Research, Kuala Lumpur 50588, Malaysia.
Chee-Onn LeongSchool of Pharmacy and Health Sciences, International Medical University, Kuala Lumpur 57000, Malaysia.
David Philip Lanep53 Laboratory (p53Lab), Agency for Science, Technology and Research (A*STAR), 8A Biomedical Grove, Immunos, Singapore 138648, Republic of Singapore.
Alan Soo-Beng KhooMolecular Pathology Unit, Cancer Research Centre, Institute for Medical Research, Kuala Lumpur 50588, Malaysia.
Institute for Medical Research · MYAgency for Science, Technology and Research · SGInternational Medical University · MYUniversity of Malaya · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The small-molecule inhibitor of p53-Mdm2 interaction, Nutlin-3, is known to be effective against cancers expressing wild-type (wt) p53. p53 mutations are rare in nasopharyngeal carcinoma (NPC), hence targeting disruption of p53-Mdm2 interaction to reactivate p53 may offer a promising therapeutic strategy for NPC. In the present study, the effects of Nutlin-3 alone or in combination with cisplatin, a standard chemotherapeutic agent, were tested on C666-1 cells, an Epstein-Barr virus (EBV)-positive NPC cell line bearing wt p53. Treatment with Nutlin-3 activated the p53 pathway and sensitized NPC cells to the cytotoxic effects of cisplatin. The combined treatment also markedly suppressed soft agar colony growth formation and increased apoptosis of NPC cells. The effect of Nutlin-3 on NPC cells was inhibited by knockdown of p53, suggesting that its effect was p53-dependent. Extended treatment with increasing concentrations of Nutlin-3 did not result in emergence of p53 mutations in the C666-1 cells. Collectively, the present study revealed supportive evidence of the effectiveness of combining cisplatin and Nutlin-3 as a potential therapy against NPC.

Indexed as

ApoptosisCarcinomaCell Line, TumorCisplatinDrug Resistance, NeoplasmGene Knockdown TechniquesHumansImidazolesNasopharyngeal CarcinomaNasopharyngeal NeoplasmsPiperazinesProto-Oncogene Proteins c-mdm2Signal TransductionTumor Suppressor Protein p53CisplatinImidazolesMDM2 protein, humannutlin 3PiperazinesProto-Oncogene Proteins c-mdm2TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID26252575
PMCPMC4564086
OpenAlexW2170580929

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.