Evidence map›Paper›PMID 24317508›Full record

ArticleOncogene2014

p21Waf1/Cip1 deficiency causes multiple mitotic defects in tumor cells.

N-N Kreis, M Sanhaji, M A Rieger, F Louwen, J Yuan

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. 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
2.9field-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

34 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Twenty years of merotelic kinetochore attachments: a historical perspective.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023
    Review
  3. Revisiting the Function of p21International journal of molecular sciences · 2022
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The p53/p73 - p21Oncogene · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. The Cell Cycle Inhibitors p21Neoplasia (New York, N.Y.) · 2017
    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

5 authors at 2 institutions in 1 country.

N-N KreisDepartment of Gynecology and Obstetrics, Frankfurt, Germany.
M SanhajiDepartment of Gynecology and Obstetrics, Frankfurt, Germany.
M A Rieger1] Department of Hematology/Oncology, J W Goethe-University, Theodor-Stern-Kai 7, Frankfurt, Germany [2] Georg-Speyer-Haus, Frankfurt, Germany [3] German Cancer Consortium (DKTK), Heidelberg, Germany [4] German Cancer Research Center (DKFZ), Heidelberg, Germany.
F LouwenDepartment of Gynecology and Obstetrics, Frankfurt, Germany.
J YuanDepartment of Gynecology and Obstetrics, Frankfurt, Germany.
Goethe University Frankfurt · DEUniversity Hospital Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a multifaceted molecule, p21 plays multiple critical roles in cell cycle regulation, differentiation, apoptosis, DNA repair, senescence, aging and stem cell reprogramming. The important roles of p21 in the interphase of the cell cycle have been intensively investigated. The function of p21 in mitosis has been proposed but not systematically studied. We show here that p21 is abundant in mitosis and binds to and inhibits the activity of Cdk1/cyclin B1. Deficiency of p21 prolongs the duration of mitosis by extending metaphase, anaphase and cytokinesis. The activity of Aurora B is reduced and the localization of Aurora B on the central spindle is disturbed in anaphase cells without p21. Moreover, HCT116 p21-/-, HeLa and Saos-2 cells depleted of p21 encounter problems in chromosome segregation and cytokinesis. Gently inhibiting the mitotic Cdk1 or add-back of p21 rescues segregation defect in HCT116 p21-/- cells. Our data demonstrate that p21 is important for a fine-tuned control of the Cdk1 activity in mitosis, and its proper function facilitates a smooth mitotic progression. Given that p21 is downregulated in the majority of tumors, either by the loss of tumor suppressors like p53 or by hyperactive oncogenes such as c-myc, this finding also sheds new light on the molecular mechanisms by which p21 functions as a tumor suppressor.

Indexed as

Aurora Kinase BCell Line, TumorCyclin B1Cyclin-Dependent Kinase Inhibitor p21HCT116 CellsHeLa CellsHumansMCF-7 CellsMitosisNeoplasmsProtein BindingAURKB protein, humanAurora Kinase BCCNB1 protein, humanCDKN1A protein, humanCyclin B1Cyclin-Dependent Kinase Inhibitor p21

Identifiers

PMID24317508
OpenAlexW2072268939

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.