Evidence map›Paper›PMID 35508987›Full record

ArticleMolecular medicine (Cambridge, Mass.)2022

NDR1 increases NOTCH1 signaling activity by impairing Fbw7 mediated NICD degradation to enhance breast cancer stem cell properties.

Ling-Ling Wang, Xiao-Yun Wan, Chun-Qi Liu, Fei-Meng Zheng

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Prognostic and predictive impact of NOTCH1 in early breast cancer.Breast cancer research and treatment · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Targeting Breast Cancer Stem Cells.International journal of biological sciences · 2023
    Review
  12. 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

4 authors at 3 institutions in 1 country.

Ling-Ling Wang *Department of Medical Oncology of The Eastern Hospital, The First Affiliated Hospital, Sun Yat-Sen University, No.58, Zhong Shan Er Lu, Guangzhou, 510080, China.
Xiao-Yun Wan *Department of Medical Oncology, Guangzhou Panyu Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China.
Chun-Qi LiuDepartment of Thoracic Surgery, Panyu Central Hospital, Guangzhou, China.
Fei-Meng ZhengDepartment of Medical Oncology of The Eastern Hospital, The First Affiliated Hospital, Sun Yat-Sen University, No.58, Zhong Shan Er Lu, Guangzhou, 510080, China. zhengfeimeng@gmail.com.ORCID 0000-0001-8793-6677
Sun Yat-sen University · CNGuangzhou University of Chinese Medicine · CNPanyu District Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe existence of breast cancer stem cells (BCSCs) causes tumor relapses, metastasis and resistance to conventional therapy in breast cancer. NDR1 kinase, a component of the Hippo pathway, plays important roles in multiple biological processes. However, its role in cancer stem cells has not been explored. The purpose of this study was to investigate the roles of NDR1 in modulating BCSCs.

methodsThe apoptosis was detected by Annexin V/Propidium Iodide staining and analyzed by flow cytometry. BCSCs were detected by CD24/44 or ALDEFLUOR staining and analyzed by flow cytometry. The proliferation ability of BCSCs was evaluated by sphere formation assay. The expression of interested proteins was detected by western blot analysis. The expression of HES-1 and c-MYC was detected by real-time PCR. Notch1 signaling activation was detected by luciferase reporter assay. Protein interaction was evaluated by immunoprecipitation. Protein degradation was evaluated by ubiquitination analysis. The clinical relevance of NDR1 was analyzed by Kaplan-Meier Plotter.

resultsNDR1 regulates apoptosis and drug resistance in breast cancer cells. The upregulation of NDR1 increases CD24

conclusionOur study revealed a novel function of NDR1 in regulating BCSC properties by activating the Notch pathway. These data might provide a potential strategy for eradicating BCSC to overcome tumor relapses, metastasis and drug resistance.

Indexed as

Biological PhenomenaBreast NeoplasmsProtein Serine-Threonine KinasesCell Line, TumorCell ProliferationFemaleHumansNeoplasm Recurrence, LocalNeoplastic Stem CellsReceptor, Notch1Signal TransductionNOTCH1 protein, humanProtein Serine-Threonine KinasesReceptor, Notch1STK38 protein, humanBreast cancerCancer stem cellFbw7NDR1NOTCH signaling

Identifiers

PMID35508987
PMCPMC9066784
OpenAlexW4225374956

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.