Evidence map›Paper›PMID 30814639›Full record

ArticleScientific reports2019

RAE1 mediated ZEB1 expression promotes epithelial-mesenchymal transition in breast cancer.

Ji Hoon Oh, Ji-Yeon Lee, Sungsook Yu, Yejin Cho, Sumin Hur, Ki Taek Nam, Myoung Hee Kim

Abstract read
In one paragraph

Article in Scientific reports, 2019. 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
–field-weighted citation impact
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.

  1. Review
  2. Subtype-Specific mInternational journal of molecular sciences · 2026
    Article
  3. Article
  4. Review
  5. Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Structure and Function of the Nuclear Pore Complex.Cold Spring Harbor perspectives in biology · 2022
    Review
  10. Article
  11. Article
  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

7 authors.

Ji Hoon OhDepartment of Anatomy, Embryology Laboratory, Yonsei University College of Medicine, Seoul, 03722, Korea.
Ji-Yeon LeeDepartment of Anatomy, Embryology Laboratory, Yonsei University College of Medicine, Seoul, 03722, Korea.
Sungsook YuSeverance Biomedical Science Institute and Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, 03722, Korea.
Yejin ChoSeverance Biomedical Science Institute and Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, 03722, Korea.
Sumin HurSeverance Biomedical Science Institute and Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, 03722, Korea.
Ki Taek NamSeverance Biomedical Science Institute and Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, 03722, Korea. kitaek@yuhs.ac.
Myoung Hee KimDepartment of Anatomy, Embryology Laboratory, Yonsei University College of Medicine, Seoul, 03722, Korea. mhkim1@yuhs.ac.ORCID 0000-0001-5652-1452

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer metastasis accounts for most of the deaths from breast cancer. Since epithelial-mesenchymal transition (EMT) plays an important role in promoting metastasis of cancer, many mechanisms regarding EMT have been studied. We previously showed that Ribonucleic acid export 1 (RAE1) is dysregulated in breast cancer and its overexpression leads to aggressive breast cancer phenotypes by inducing EMT. Here, we evaluated the functional capacity of RAE1 in breast cancer metastasis by using a three-dimensional (3D) culture system and xenograft models. Furthermore, to investigate the mechanisms of RAE1-driven EMT, in vitro studies were carried out. The induction of EMT with RAE1-overexpression was confirmed under the 3D culture system and in vivo system. Importantly, RAE1 mediates upregulation of an EMT marker ZEB1, by binding to the promoter region of ZEB1. Knockdown of ZEB1 in RAE1-overexpressing cells suppressed invasive and migratory behaviors, accompanied by an increase in epithelial and a decrease in mesenchymal markers. Taken together, these data demonstrate that RAE1 contributes to breast cancer metastasis by regulating a key EMT-inducing factor ZEB1 expression, suggesting its potential as a therapeutic target.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorEpithelial-Mesenchymal TransitionFemaleGene ExpressionHeterograftsHomeodomain ProteinsHumansMCF-7 CellsMiceMice, Inbred BALB CMice, NudeMicroRNAsNuclear Matrix-Associated ProteinsNucleocytoplasmic Transport ProteinsHomeodomain ProteinsMicroRNAsNuclear Matrix-Associated ProteinsNucleocytoplasmic Transport ProteinsRAE1 protein, humanTranscription FactorsZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID30814639
PMCPMC6393568

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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.