Evidence map›Paper›PMID 31547193›Full record

ReviewCells2019

The E-Cadherin and N-Cadherin Switch in Epithelial-to-Mesenchymal Transition: Signaling, Therapeutic Implications, and Challenges.

Chin-Yap Loh, Jian Yi Chai, Ting Fang Tang, Won Fen Wong, Gautam Sethi, Muthu Kumaraswamy Shanmugam, Pei Pei Chong, Chung Yeng Looi

Abstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 778 papers.

0numbers the graph read from it
0cells of the map it votes in
778citing 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

778 citing papers in PubMed.

  1. Article
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  6. FASEB bioAdvances · 2026
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  9. MXRA5 promotes the progression and metastasis of breast cancerThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
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  13. Review
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  17. Beyond the gap: moonlighting functions of connexins in cancer.Cell communication and signaling : CCS · 2026
    Review
  18. Article
  19. Article
  20. Article

718 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

8 authors.

Chin-Yap LohSchool of Biosciences, Faculty of Health and Medical Sciences, Taylor's University, Subang Jaya 47500, Malaysia. cyloh5@gmail.com.
Jian Yi ChaiSchool of Biosciences, Faculty of Health and Medical Sciences, Taylor's University, Subang Jaya 47500, Malaysia. benjaminchaijy@gmail.com.
Ting Fang TangDepartment of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia. tiffanytftang@gmail.com.
Won Fen WongDepartment of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia. wonfen@um.edu.my.ORCID 0000-0003-1082-1956
Gautam SethiDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore. phcgs@nus.edu.sg.
Muthu Kumaraswamy ShanmugamDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore. phcsmk@nus.edu.sg.
Pei Pei ChongSchool of Biosciences, Faculty of Health and Medical Sciences, Taylor's University, Subang Jaya 47500, Malaysia. peipei.chong@taylors.edu.my.ORCID 0000-0002-8229-3593
Chung Yeng LooiSchool of Biosciences, Faculty of Health and Medical Sciences, Taylor's University, Subang Jaya 47500, Malaysia. chungyeng.looi@taylors.edu.my.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-to-Mesenchymal Transition (EMT) has been shown to be crucial in tumorigenesis where the EMT program enhances metastasis, chemoresistance and tumor stemness. Due to its emerging role as a pivotal driver of tumorigenesis, targeting EMT is of great therapeutic interest in counteracting metastasis and chemoresistance in cancer patients. The hallmark of EMT is the upregulation of N-cadherin followed by the downregulation of E-cadherin, and this process is regulated by a complex network of signaling pathways and transcription factors. In this review, we summarized the recent understanding of the roles of E- and N-cadherins in cancer invasion and metastasis as well as the crosstalk with other signaling pathways involved in EMT. We also highlighted a few natural compounds with potential anti-EMT property and outlined the future directions in the development of novel intervention in human cancer treatments. We have reviewed 287 published papers related to this topic and identified some of the challenges faced in translating the discovery work from bench to bedside.

Indexed as

Genes, SwitchAnimalsAntineoplastic AgentsCadherinsCarcinogenesisDrug DiscoveryEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyMultigene FamilySignal TransductionAntineoplastic AgentsCadherinsE-cadherinEpithelial-to-Mesenchymal Transitionnatural compoundsN-cadherinsignaling pathways

Identifiers

PMID31547193
PMCPMC6830116

What OpenQuestion holds

Textmetadata
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.