Evidence map›Paper›PMID 24168186›Full record

ReviewCurrent cancer drug targets2013

The Role of Snail in EMT and Tumorigenesis.

Yifan Wang, Jian Shi, Kequn Chai, Xuhua Ying, Binhua P Zhou

Abstract readReview
In one paragraph

Review in Current cancer drug targets, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 540 papers.

0numbers the graph read from it
0cells of the map it votes in
540citing 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

540 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Loss of Twist1 leads to disruption of ciliary length, endocytic vesicle dynamics, and cell-cell junctions during neural tube formation.Developmental dynamics : an official publication of the American Association of Anatomists · 2026
    Article

480 more citing papers are in PubMed but not listed here.

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.

Yifan Wang *Departments of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky School of Medicine, Lexington, KY, 40506, United States.
Jian Shi *Departments of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky School of Medicine, Lexington, KY, 40506, United States.
Kequn ChaiCancer Institute of Integrative Medicine, Zhejiang Academy of Chinese Medicine, Hangzhou, Zhejiang.
Xuhua YingCancer Institute of Integrative Medicine, Zhejiang Academy of Chinese Medicine, Hangzhou, Zhejiang.
Binhua P ZhouDepartments of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky School of Medicine, Lexington, KY, 40506, United States.

Funding

Regulation of Snail in breast cancer progression and metastasisR01CA125454 · NCI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI ZHOU, BINHUA P · 2007 to 2017
$2.8M
NCI NIH HHS 2R01CA125454NCI NIH HHS R01 CA125454
6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is a highly conserved process in which polarized, immobile epithelial cells lose tight junctions, associated adherence, and become migratory mesenchymal cells. Several transcription factors, including the Snail/Slug family, Twist, δEF1/ZEB1, SIP1/ZEB2 and E12/E47 respond to microenvironmental stimuli and function as molecular switches for the EMT program. Snail is a zinc-finger transcriptional repressor controlling EMT during embryogenesis and tumor progression. Through its N-terminal SNAG domain, Snail interacts with several corepressors and epigenetic remodeling complexes to repress specific target genes, such as the E-cadherin gene (CDH1). An integrated and complex signaling network, including the RTKs, TGF-β, Notch, Wnt, TNF-α, and BMPs pathways, activates Snail, thereby inducing EMT. Snail expression correlates with the tumor grade, nodal metastasis of many types of tumor and predicts a poor outcome in patients with metastatic cancer. Emerging evidences indicate that Snail causes a metabolic reprogramming, bestows tumor cells with cancer stem cell-like traits, and additionally, promotes drug resistance, tumor recurrence and metastasis. Despite many new and exciting developments, several challenges remain to be addressed in order to understand more thoroughly the role of Snail in metastasis. Additional investigations are required to disclose the contribution of microenvironmental factors on tumor progression. This information will lead to a comprehensive understanding of Snail in cancer and will provide us with novel approaches for preventing and treating metastatic cancers.

Indexed as

CarcinogenesisEpithelial-Mesenchymal TransitionHumansNeoplasm MetastasisSignal TransductionSnail Family Transcription FactorsTranscription FactorsTumor MicroenvironmentSNAI1 protein, humanSnail Family Transcription FactorsTranscription Factors

Identifiers

PMID24168186
PMCPMC4004763

What OpenQuestion holds

Textmetadata
LicenceTDM
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.