Evidence map›Paper›PMID 28806397›Full record

ArticleOncogene2017

Mdm2 promotes Cdc25C protein degradation and delays cell cycle progression through the G2/M phase.

L E Giono, L Resnick-Silverman, L A Carvajal, S St Clair, J J Manfredi

Abstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.7field-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

34 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Fumonisin BToxins · 2021
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. 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

5 authors at 1 institution in 1 country.

L E GionoDepartment of Oncological Sciences and Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
L Resnick-SilvermanDepartment of Oncological Sciences and Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
L A CarvajalDepartment of Oncological Sciences and Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
S St ClairDepartment of Oncological Sciences and Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
J J ManfrediDepartment of Oncological Sciences and Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Icahn School of Medicine at Mount Sinai · US

Funding

THE TISCH CANCER INSTITUTE - CANCER CENTER SUPPORT GRANTP30CA196521 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Ramon E Parsons · 2015 to 2026
$35.4M
Modeling Mdm2- and 12q amplicon-driven sarcomaR03CA216466 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MANFREDI, JAMES J · 2017 to 2018
$167k
Mechanisms of DNA damage-induced, p53-dependent repression of the Cdc25C PhosphatF31CA150539 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CARVAJAL, LUIS A. · 2010 to 2012
$71k
NCI NIH HHS F31 CA150539NCI NIH HHS P30 CA196521NCI NIH HHS R03 CA216466
6 · The paper itself

Abstract

Upon different types of stress, the gene encoding the mitosis-promoting phosphatase Cdc25C is transcriptionally repressed by p53, contributing to p53's enforcement of a G2 cell cycle arrest. In addition, Cdc25C protein stability is also decreased following DNA damage. Mdm2, another p53 target gene, encodes a ubiquitin ligase that negatively regulates p53 levels by ubiquitination. Ablation of Mdm2 by siRNA led to an increase in p53 protein and repression of Cdc25C gene expression. However, Cdc25C protein levels were actually increased following Mdm2 depletion. Mdm2 is shown to negatively regulate Cdc25C protein levels by reducing its half-life independently of the presence of p53. Further, Mdm2 physically interacts with Cdc25C and promotes its degradation through the proteasome in a ubiquitin-independent manner. Either Mdm2 overexpression or Cdc25C downregulation delays cell cycle progression through the G2/M phase. Thus, the repression of the Cdc25C promoter by p53, together with p53-dependent induction of Mdm2 and subsequent degradation of Cdc25C, could provide a dual mechanism by which p53 can enforce and maintain a G2/M cell cycle arrest.

Indexed as

AnimalsAntibiotics, Antineoplasticcdc25 PhosphatasesCell LineCell Line, TumorCells, CulturedDown-RegulationDoxorubicinG2 Phase Cell Cycle CheckpointsGene Expression RegulationHCT116 CellsHumansImmunoblottingMice, KnockoutProteolysisProto-Oncogene Proteins c-mdm2Antibiotics, Antineoplasticcdc25 PhosphatasesDoxorubicinMDM2 protein, humanProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53

Identifiers

PMID28806397
PMCPMC6002854
OpenAlexW2748005886

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.