Evidence map›Paper›PMID 21216934›Full record

ArticleMolecular cancer therapeutics2011

p53R2 inhibits the proliferation of human cancer cells in association with cell-cycle arrest.

Keqiang Zhang, Jun Wu, Xiwei Wu, Xiaochen Wang, Yan Wang, Ning Zhou, Mei-ling Kuo, Xiyong Liu, Bingsen Zhou, Lufen Chang and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  5. Review
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  7. δ-Catenin Participates in EGF/AKT/p21International journal of molecular sciences · 2021
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  10. Synthesis andIranian journal of pharmaceutical research : IJPR · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. E2F1 regulates p53R2 gene expression in p53-deficient cells.Molecular and cellular biochemistry · 2015
    Article
  18. Article
  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

12 authors at 1 institution in 1 country.

Keqiang ZhangDepartment of Molecular Pharmacology, Beckman Research Institute, City of Hope National Medical Center, 1500 E. Duarte Rd., Duarte, CA 91010, USA.
Jun Wu
Xiwei Wu
Xiaochen Wang
Yan Wang
Ning Zhou
Mei-ling Kuo
Xiyong Liu
Bingsen Zhou
Lufen Chang
David Ann
Yun Yen
City Of Hope National Medical Center · US

Funding

Drug Development of Ribonucleotide Reductase InhibitorR01CA127541 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI HORNE, DAVID A. · 2008 to 2012
$1.7M
NCI NIH HHS CA 127541-01NCI NIH HHS R01 CA127541
6 · The paper itself

Abstract

Deregulation of the expression of p53R2, a p53-inducible homologue of the R2 subunit of ribonucleotide reductase, has been found in various human cancer tissues; however, the roles p53R2 plays in cancer progression and malignancy remain controversial. In the present study, we examined changes in gene expression profiles associated with p53R2 in cancer cells, using the analysis of cDNA microarray. Gene set enrichment analysis identified that the gene set regulating cell-cycle progression was significantly enriched in p53R2-silencing human oropharyngeal carcinoma KB cells. Attenuation of p53R2 expression significantly reduced p21 expression and moderately increased cyclin D1 expression in both wild-type p53 cancer cells (KB and MCF-7) and mutant p53 cancer cells (PC3 and MDA-MB-231). Conversely, overexpression of p53R2-GFP resulted in an increase in the expression of p21 and decrease in the expression of cyclin D1, which correlated with reduced cell population in S-phase in vitro and suppressed growth in vivo. Furthermore, the MAP/ERK kinase inhibitor PD98059 partially abolished modulation of p21 and cyclin D1 expression by p53R2. Moreover, under the conditions of nonstress and adriamycin-induced genotoxic stress, attenuation of p53R2 in KB cells significantly increased phosphorylated H2AX, which indicates that attenuation of p53R2 may enhance DNA damage induced by adriamycin. Overall, our study shows that p53R2 may suppress cancer cell proliferation partially by upregulation of p21 and downregulation of cyclin D1; p53R2 plays critical roles not only in DNA damage repair but also in proliferation of cancer cells.

Indexed as

AnimalsCell CycleCell Cycle ProteinsCell Line, TumorCell ProliferationCyclin D1Cyclin-Dependent Kinase Inhibitor p21DNA DamageGene Expression ProfilingGene Expression Regulation, NeoplasticGene SilencingHumansKB CellsMiceMice, SCIDMitogen-Activated Protein Kinase 1CDKN1A protein, humanCell Cycle ProteinsCyclin D1Cyclin-Dependent Kinase Inhibitor p21MAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Ribonucleotide ReductasesRRM2B protein, human

Identifiers

PMID21216934
PMCPMC3042803
OpenAlexW2143391022

What OpenQuestion holds

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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.