Evidence map›Paper›PMID 33745968›Full record

ArticleThe Journal of biological chemistry

CDC25B induces cellular senescence and correlates with tumor suppression in a p53-dependent manner.

Ying-Chieh Chen, Hsi-Hsien Hsieh, Hsi-Chi Chang, Hsin-Chiao Wang, Wey-Jinq Lin, Jing-Jer Lin

Open access · goldAbstract read
In one paragraph

Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Comprehensive analysis of CDK5 as a novel biomarker for progression in esophageal cancer.Esophagus : official journal of the Japan Esophageal Society · 2023
    Article
  12. Review
  13. Article
  14. DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022
    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

6 authors at 2 institutions in 1 country.

Ying-Chieh ChenInstitute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei, Taiwan.
Hsi-Hsien HsiehInstitute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei, Taiwan.
Hsi-Chi ChangInstitute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei, Taiwan.
Hsin-Chiao WangInstitute of Biochemistry and Molecular Biology, National Taiwan University College of Medicine, Taipei, Taiwan.
Wey-Jinq LinInstitute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei, Taiwan. Electronic address: wjlin@ym.edu.tw.
Jing-Jer LinInstitute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei, Taiwan; Institute of Biochemistry and Molecular Biology, National Taiwan University College of Medicine, Taipei, Taiwan. Electronic address: jingjerlin@ntu.edu.tw.
National Yang Ming Chiao Tung University · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The phosphatase cell division cycle 25B (Cdc25B) regulates cell cycle progression. Increased Cdc25B levels are often detected in cancer cell lines and human cancers and have been implicated in contributing to tumor growth, potentially by providing cancer cells with the ability to bypass checkpoint controls. However, the specific mechanism by which increased Cdc25B impacts tumor progression is not clear. Here we analyzed The Cancer Genome Atlas (TCGA) database and found that patients with high CDC25B expression had the expected poor survival. However, we also found that high CDC25B expression had a p53-dependent tumor suppressive effect in lung cancer and possibly several other cancer types. Looking in more detail at the tumor suppressive function of Cdc25B, we found that increased Cdc25B expression caused inhibition of cell growth in human normal fibroblasts. This effect was not due to alteration of specific cell cycle stage or inhibition of apoptosis, nor by induction of the DNA damage response. Instead, increased CDC25B expression led cells into senescence. We also found that p53 was required to induce senescence, which might explain the p53-dependent tumor suppressive function of Cdc25B. Mechanistically, we found that the Cdc25B phosphatase activity was required to induce senescence. Further analysis also found that Cdc25B stabilized p53 through binding and dephosphorylating p53. Together, this study identified a tumor-suppressive function of Cdc25B that is mediated through a p53-dependent senescence pathway.

Indexed as

Cellular SenescenceCell CycleCell Line, TumorDNA DamageHumansTumor Suppressor Protein p53TP53 protein, humanTumor Suppressor Protein p53CDC25Bp53phosphatasesenescencetumor suppression

Identifiers

PMID33745968
PMCPMC8054198
OpenAlexW3139363495

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.