Evidence map›Paper›PMID 25586771›Full record

ArticleMolecular medicine reports2015

Special AT-rich sequence-binding protein-1 participates in the maintenance of breast cancer stem cells through regulation of the Notch signaling pathway and expression of Snail1 and Twist1.

Zhengkui Sun, Chao Zhang, Xuesen Zou, Guixiang Jiang, Zongquan Xu, Wenting Li, Hui Xie

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. The Role of SATB1 in Tumour Progression and Metastasis.International journal of molecular sciences · 2019
    Review
  9. Review
  10. Article
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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

7 authors at 2 institutions in 1 country.

Zhengkui SunDepartment of Breast Surgery, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029, P.R. China.
Chao ZhangDepartment of Clinical Medicine, Medical School of Nanchang University, Nanchang, Jiangxi 330029, P.R. China.
Xuesen ZouDepartment of Breast Surgery, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029, P.R. China.
Guixiang JiangDepartment of Breast Surgery, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029, P.R. China.
Zongquan XuDepartment of Breast Surgery, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029, P.R. China.
Wenting LiDepartment of Clinical Medicine, Medical School of Nanchang University, Nanchang, Jiangxi 330029, P.R. China.
Hui XieDepartment of Clinical Medicine, Medical School of Nanchang University, Nanchang, Jiangxi 330029, P.R. China.
Jiangxi Provincial Cancer Hospital · CNNanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The stem cell populations in cancerous tissues and cell lines vary widely and are often associated with aggressive cases of breast cancer. Despite research on the topic, the mechanism underlying the regulation of the breast cancer stem cell (BCSC) population within tumors remains to be fully elucidated. To investigate the function of special AT‑rich sequence‑binding protein‑1 (SATB1) in the maintenance of the BCSC population, SATB1 was overexpressed with lentivirus in MCF‑7 cells or knocked down with shRNA‑lentivirus in BT‑549 cells. The effects of SATB1 overexpression or knockdown on mammosphere formation, the size of the of BCSC population, cell invasion and tumorigenesis were investigated. Activation of the Notch signaling pathway and expression of Snail1 and Twist1 were also examined in the cells. Overexpression of SATB1 in MCF‑7 cells was observed to increase mammosphere formation, the size of the BCSC population, cell invasion and tumorigenesis, accompanied by an increase in the activation of Notch signaling and expression levels of Snail1 and Twist1. Conversely, knockdown of SATB1 in BT‑549 cells produced the opposite effects. The results indicated that expression of SATB1 may increase the size of the BCSC population via the activation of the Notch signaling pathway and by increasing expression levels of Snail1 and Twist1.

Indexed as

Cell Self RenewalGene Expression Regulation, NeoplasticAnimalsBreast NeoplasmsCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalFemaleGene ExpressionGene Knockdown TechniquesHeterograftsHumansHyaluronan ReceptorsImmunophenotypingMatrix Attachment Region Binding ProteinsMCF-7 CellsHyaluronan ReceptorsMatrix Attachment Region Binding ProteinsNuclear ProteinsReceptors, NotchSATB1 protein, humanSNAI1 protein, humanSnail Family Transcription FactorsTranscription FactorsTWIST1 protein, humanTwist-Related Protein 1

Identifiers

PMID25586771
PMCPMC4368071
OpenAlexW2142577487

What OpenQuestion holds

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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.