Evidence map›Paper›PMID 28262781›Full record

ArticleScientific reports2017

WEE1 inhibition targets cell cycle checkpoints for triple negative breast cancers to overcome cisplatin resistance.

Hongping Zheng, Fangyuan Shao, Scots Martin, Xiaoling Xu, Chu-Xia Deng

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 57 citations in OpenAlex.

  1. Trial
  2. Review
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  5. Article
  6. MRCK as a Potential Target for Claudin-Low Subtype of Breast Cancer.International journal of biological sciences · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Targeting replication stress in cancer therapy.Nature reviews. Drug discovery · 2023
    Review
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  20. New Insights into Therapy-Induced Progression of Cancer.International journal of molecular sciences · 2020
    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

5 authors at 3 institutions in 2 countries.

Hongping ZhengGenetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, USA.
Fangyuan ShaoFaculty of Health Sciences, University of Macau, Macau SAR, China.
Scots MartinDivision of Pre-Clinical Innovation, National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, USA.
Xiaoling XuFaculty of Health Sciences, University of Macau, Macau SAR, China.
Chu-Xia DengGenetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, USA.
University of Macau · MONational Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin is one of the most commonly used therapeutic drugs for cancer therapy, yet prolonged cisplatin treatment frequently results in drug resistance. To enhance therapeutic effect of cisplatin, we conducted a high throughput screening using a kinase library containing 704 kinases against triple negative breast cancer (TNBC) cells. We demonstrated that cisplatin activates ATR, CHK1 and WEE1, which shut down DNA replication and attenuate cisplatin induced-lethality. WEE1 inhibition sensitizes TNBCs and cisplatin resistant cancer cells to cisplatin-induced lethality, because it not only impairs DNA replication checkpoint more profoundly than inhibition of ATR or CHK1, but also defects G2-M cell cycle checkpoint. Finally, we demonstrated that combined cisplatin treatment and WEE1 inhibition synergistically inhibits xenograft cancer growth accompanied by markedly reduced expression of TNBC signature genes. Thus targeting DNA replication and G2-M cell cycle checkpoint simultaneously by cisplatin and WEE1 inhibition is promising for TNBCs treatment, and for overcoming their cisplatin resistance.

Indexed as

AnimalsAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsCell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorCheckpoint Kinase 1CisplatinDisease Models, AnimalDNA DamageDNA ReplicationDrug Resistance, NeoplasmFemaleHumansMiceMolecular Targeted TherapyAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsATR protein, humanCell Cycle ProteinsCheckpoint Kinase 1CisplatinNuclear ProteinsProtein-Tyrosine KinasesWEE1 protein, human

Identifiers

PMID28262781
PMCPMC5338009
OpenAlexW2594438232

What OpenQuestion holds

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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.