Evidence map›Paper›PMID 15361831›Full record

ArticleOncogene2004

Survivin regulates the p53 tumor suppressor gene family.

Zhanxiang Wang, Seiji Fukuda, Louis M Pelus

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Antitumoral effects of γCdcPLI, a PLAScientific reports · 2017
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Survivin splice variants and their diagnostic significance.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Review
  18. Article
  19. Survivin: A molecular biomarker in cancer.The Indian journal of medical research · 2015
    Review
  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

3 authors at 2 institutions in 1 country.

Zhanxiang WangDepartment of Microbiology and Immunology and The Walther Oncology Center, Indiana University School of Medicine, 950 West Walnut Street, Indianapolis, IN 46202, USA.
Seiji Fukuda
Louis M Pelus
Indiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Role of Survivin in Blood Stem Cell Cycle and ApoptosisR01HL079654 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI PELUS, LOUIS M · 2004 to 2007
$1.3M
NHLBI NIH HHS HL079654
6 · The paper itself

Abstract

Survivin regulates cell division and inhibits apoptosis by blocking caspase activation. The tumor suppressor p53 inhibits cell cycle progression and induces apoptosis. Since Survivin overexpression and loss of wild-type p53 expression/function occur in most cancers, we investigated whether Survivin regulates p53. Stable overexpression of Survivin protects BaF3 cells from Adriamycin-induced apoptosis, while dominant-negative (T34A) and antisense (AS) Survivin accelerate apoptosis. In BaF3 cells and transiently transfected MCF7 breast cancer cells, elevation of total and phospho-Ser15-p53 in response to Adriamycin is blocked by Survivin and enhanced by Survivin disruption. Furthermore, in Adriamycin-treated MCF7 cells, ectopic Survivin decreased p53 mRNA and increased mRNA and protein of the p53 homologues DeltaNp63 and TAp73 and mRNA for DeltaNp73, suggesting that Survivin may differentially regulate p53 family transcription. Concomitant with decreasing p53 mRNA, Survivin decreased Mdm2 mRNA. Survivin disruption by T34A or AS Survivin resulted in reduced Mdm2 protein. The caspase inhibitor, Z-VAD-FMK, blocked the decrease in Mdm2 as well as the increase in p53 resulting from Survivin disruption, indicating that Survivin regulates Mdm2 at the post-translational level. Proteosome inhibition confirmed that reduced p53 protein observed in cells overexpressing Survivin is due to enhanced p53 degradation resulting from Survivin-mediated inhibition of Mdm2 cleavage by caspases. In summary, our results identify regulatory interactions between Survivin and p53 at the mRNA and protein levels, and suggest that the p53 homologues DeltaNp63, TAp73 and DeltaNp73 may also be regulated by Survivin.

Indexed as

Gene Expression RegulationGenes, p53AnimalsApoptosisCaspase InhibitorsDNA-Binding ProteinsDoxorubicinGenes, Tumor SuppressorHumansInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsNeoplasm ProteinsNuclear ProteinsPhosphoproteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2BIRC5 protein, humanCaspase Inhibitorsdelta Np73 protein, humanDNA-Binding ProteinsDoxorubicinInhibitor of Apoptosis ProteinsMDM2 protein, humanMicrotubule-Associated ProteinsNeoplasm ProteinsNuclear ProteinsPhosphoproteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2SurvivinTP63 protein, humanTrans-ActivatorsTranscription FactorsTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID15361831
OpenAlexW2011590696

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.