Evidence map›Paper›PMID 28827448›Full record

ArticleThe Journal of experimental medicine2017

EGF hijacks miR-198/FSTL1 wound-healing switch and steers a two-pronged pathway toward metastasis.

Gopinath M Sundaram, Hisyam M Ismail, Mohsin Bashir, Manish Muhuri, Candida Vaz, Srikanth Nama, Ghim Siong Ow, Ivshina Anna Vladimirovna, Rajkumar Ramalingam, Brian Burke and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
  2. Unleashing Wnts: Wnt Ligands Fuel Cancer Spread.Journal of cancer biology · 2025
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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

14 authors at 1 institution in 1 country.

Gopinath M SundaramInstitute of Medical Biology, Agency for Science, Technology, and Research (A*STAR), Singapore.ORCID http://orcid.org/0000-0002-8074-6624
Hisyam M IsmailInstitute of Medical Biology, Agency for Science, Technology, and Research (A*STAR), Singapore.
Mohsin BashirInstitute of Medical Biology, Agency for Science, Technology, and Research (A*STAR), Singapore.
Manish MuhuriInstitute of Medical Biology, Agency for Science, Technology, and Research (A*STAR), Singapore.ORCID http://orcid.org/0000-0003-3265-903X
Candida VazBioinformatics Institute, Agency for Science, Technology, and Research (A*STAR), Singapore.ORCID http://orcid.org/0000-0002-6650-7889
Srikanth NamaInstitute of Medical Biology, Agency for Science, Technology, and Research (A*STAR), Singapore.
Ghim Siong OwBioinformatics Institute, Agency for Science, Technology, and Research (A*STAR), Singapore.
Ivshina Anna VladimirovnaBioinformatics Institute, Agency for Science, Technology, and Research (A*STAR), Singapore.
Rajkumar RamalingamInstitute of Medical Biology, Agency for Science, Technology, and Research (A*STAR), Singapore.
Brian BurkeInstitute of Medical Biology, Agency for Science, Technology, and Research (A*STAR), Singapore.
Vivek TanavdeBioinformatics Institute, Agency for Science, Technology, and Research (A*STAR), Singapore.
Vladimir KuznetsovBioinformatics Institute, Agency for Science, Technology, and Research (A*STAR), Singapore.
E Birgitte LaneInstitute of Medical Biology, Agency for Science, Technology, and Research (A*STAR), Singapore.
Prabha SampathInstitute of Medical Biology, Agency for Science, Technology, and Research (A*STAR), Singapore prabha.sampath@imb.a-star.edu.sg.ORCID http://orcid.org/0000-0001-8672-498X
Agency for Science, Technology and Research · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial carcinomas are well known to activate a prolonged wound-healing program that promotes malignant transformation. Wound closure requires the activation of keratinocyte migration via a dual-state molecular switch. This switch involves production of either the anti-migratory microRNA miR-198 or the pro-migratory follistatin-like 1 (FSTL1) protein from a single transcript; miR-198 expression in healthy skin is down-regulated in favor of FSTL1 upon wounding, which enhances keratinocyte migration and promotes re-epithelialization. Here, we reveal a defective molecular switch in head and neck squamous cell carcinoma (HNSCC). This defect shuts off miR-198 expression in favor of sustained FSTL1 translation, driving metastasis through dual parallel pathways involving DIAPH1 and FSTL1. DIAPH1, a miR-198 target, enhances directional migration through sequestration of Arpin, a competitive inhibitor of Arp2/3 complex. FSTL1 blocks Wnt7a-mediated repression of extracellular signal-regulated kinase phosphorylation, enabling production of MMP9, which degrades the extracellular matrix and facilitates metastasis. The prognostic significance of the FSTL1-DIAPH1 gene pair makes it an attractive target for therapeutic intervention.

Indexed as

AnimalsBlotting, WesternCarcinoma, Squamous CellCell ProliferationCell Transformation, NeoplasticEpidermal Growth FactorFemaleFollistatin-Related ProteinsGenes, SwitchHead and Neck NeoplasmsImmunoprecipitationMass SpectrometryMice, Inbred NODMicroRNAsWound HealingEpidermal Growth FactorFollistatin-Related ProteinsFstl1 protein, mouseMicroRNAsMIRN198 microRNA, humanMIRN198 microRNA, mouse

Identifiers

PMID28827448
PMCPMC5626400
OpenAlexW2747073619

What Socratic 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 Socratic graph.